Database Query Results : Resveratrol, ,

RES, Resveratrol: Click to Expand ⟱
Features: polyphenol
Found in red grapes and products made with grapes.
Resveratrol is a polyphenol compound found in various plant species, including grapes, berries, and peanuts.
• Anti-inflammatory effects, Antioxidant effects:
- Antiplatelet aggregation for stroke prevention
- BioAvialability use piperine
- some sources may use Japanese knotweed roots (Reynoutria Japonica - root) as source which might contain Emodin (laxative)
-known as Nrf2 activator, both in cancer and normal cells. Which raises controversity of use in ROS↑ therapies. Interestingly there are reports of NRF2↑ and ROS↑ in cancer cells. This raises the question of if it is a chemosensitizer. However other reports indicate NRF2 droping with Res, indicating it maybe a chemosenstizer.
- RES is also considered to be them most effective natural SIRT1↑ -activating compound (STACs).

However, in the presence of certain metals, such as copper or iron, resveratrol can undergo a process called Fenton reaction, which can lead to the generation of reactive oxygen species (ROS). The pro-oxidant effects of resveratrol are often observed at high concentrations, typically above 50-100 μM, and in the presence of certain metals or other pro-oxidant agents. In contrast, the antioxidant effects of resveratrol are typically observed at lower concentrations, typically below 10-20 μM.

Clinical trials have used doses ranging from 150 mg to 5 grams per day. Lower doses (< 1 g/day) are often well-tolerated, but higher doses might be necessary for therapeutic effects and can be associated with side effects.

-Note half-life 1-3 hrs?.
BioAv poor: min 5uM/L required for chemopreventive effects, but 25mg Oral only yeilds 20nM. co-administration of piperine
Pathways:
- usually induce ROS production in cancer cells, while reducing ROS in normal cells.
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓,
- Lowers AntiOxidant defense in Cancer Cells: NRF2(typically increased), TrxR↓**, SOD↓, GSH↓ Catalase↓ HO1↓(wrong direction), GPx↓
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : NLRP3↓, IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, TIMP2, IGF-1↓, uPA↓, VEGF↓, ROCK1↓, FAK↓, RhoA↓, NF-κB↓, CXCR4↓, SDF1↓, TGF-β↓, α-SMA↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, EZH2↓, P53↑, HSP↓, Sp proteins↓,
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓, FAK↓, ERK↓, EMT↓, TOP1↓, TET1↓,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, PFKs↓, PDKs↓, ECAR↓, OXPHOS↓, GRP78↑, Glucose↓, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, FGF↓, PDGF↓, EGFR↓, Integrins↓,
- inhibits Cancer Stem Cells : CSC↓, CK2↓, Hh↓, CD133↓, CD24↓, β-catenin↓, sox2↓, notch2↓, nestin↓, OCT4↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK, ERK↓, JNK,
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells


Scientific Papers found: Click to Expand⟱
2578- ART/DHA,  RES,    Synergic effects of artemisinin and resveratrol in cancer cells
- in-vitro, Liver, HepG2 - in-vitro, Cerv, HeLa
"highlight2" >Dose↝, The combination of ART and Res exhibited the strongest anticancer effect at the ratio of 1:2 (ART to Res).
"highlight2" >TumCMig↓, combination of the two drugs also markedly reduced the ability of cell migration
"highlight2" >Apoptosis↑, Apoptosis analysis showed that combination of ART and Res significantly increased the apoptosis and necrosis rather than use singly
"highlight2" >necrosis↑,
"highlight2" >ROS↑, ROS levels were elevated by combining ART with Res.
"highlight2" >eff↑, the data suggested that the IC50 of the combination of ART and Res is lower than that of each drug used alone.

1383- CUR,  BBR,  RES,    Regulation of GSK-3 activity by curcumin, berberine and resveratrol: Potential effects on multiple diseases
- Review, NA, NA
"highlight2" >GSK‐3β↝,
"highlight2" >ROS↑, BBB increased ROS production by decreasing c-MYC expression

3748- CUR,  RES,  Hup,  Riv,  Gala  Natural acetylcholinesterase inhibitors: A multi-targeted therapeutic potential in Alzheimer's disease
- Review, AD, NA
"highlight2" >*AChE↓, natural phytocompounds such as Curcumin, Varenicline, Huperrtzine, Resveratrol, and Cycloastrageno have received FDA approval to treat Alzheimer's disease
"highlight2" >*Inflam↓, Anti-amyloidogenic, anti-inflammatory, anti-ChE, anti – secretase
"highlight2" >*Aβ↓, Prevent cognitive impairment and associated oxidative stress by reducing plaque formation
"highlight2" >*cognitive↑,
"highlight2" >*ROS↓,

3862- CUR,  RES,    The metalloproteinase ADAM10: A useful therapeutic target?
- Review, AD, NA
"highlight2" >*SIRT1↑, Therefore, the Sirt1 activators curcumin and resveratrol are tested for their clinical impact on ADAM10 expression in AD.
"highlight2" >*ADAM10↑,

128- CUR,  RES,    Evaluation of biophysical as well as biochemical potential of curcumin and resveratrol during prostate cancer
- in-vivo, Pca, NA
"highlight2" >lipid-P↓,

134- CUR,  RES,  MEL,  SIL,    Thioredoxin 1 modulates apoptosis induced by bioactive compounds in prostate cancer cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, PC3
"highlight2" >Apoptosis↑,
"highlight2" >ROS↑,
"highlight2" >Trx1↓,

182- CUR,  RES,  GI,    Chemopreventive anti-inflammatory activities of curcumin and other phytochemicals mediated by MAP kinase phosphatase-5 in prostate cells
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP - in-vitro, Pca, LAPC-4
"highlight2" >p38↓,
"highlight2" >MKP5↑,

872- CUR,  RES,    New Insights into Curcumin- and Resveratrol-Mediated Anti-Cancer Effects
- in-vitro, BC, TUBO - in-vitro, BC, SALTO
"highlight2" >TumCP↓,
"highlight2" >tumCV↓,
"highlight2" >p62↓, reduced by Cur
"highlight2" >p62↑, accumulated by Res
"highlight2" >TumAuto↑, Cur only
"highlight2" >TumAuto↓, Res only
"highlight2" >ROS↑, increased ROS with Res
"highlight2" >ROS↓, decreased ROS with Cur or combination
"highlight2" >CHOP↑, strongly upregulated by the curcumin/resveratrol combination

685- EGCG,  CUR,  SFN,  RES,  GEN  The “Big Five” Phytochemicals Targeting Cancer Stem Cells: Curcumin, EGCG, Sulforaphane, Resveratrol and Genistein
- Analysis, NA, NA
"highlight2" >Bcl-2↓,
"highlight2" >survivin↓,
"highlight2" >XIAP↓,
"highlight2" >EMT↓,
"highlight2" >Apoptosis↑,
"highlight2" >Nanog↓,
"highlight2" >cMyc↓,
"highlight2" >OCT4↓,
"highlight2" >Snail↓,
"highlight2" >Slug↓,
"highlight2" >Zeb1↓,
"highlight2" >TCF↓,

1534- LT,  Api,  EGCG,  RES,    Plant polyphenol induced cell death in human cancer cells involves mobilization of intracellular copper ions and reactive oxygen species generation: a mechanism for cancer chemopreventive action
- in-vitro, Nor, MCF10 - in-vitro, BC, MDA-MB-231 - in-vitro, BC, MDA-MB-468 - in-vitro, PC, Bxpc-3
"highlight2" >TumCP↓,
"highlight2" >Apoptosis↑,
"highlight2" >eff↓, cell death is prevented to a significant extent by cuprous chelator neocuproine and reactive oxygen species scavengers
"highlight2" >*toxicity↑, normal breast epithelial cells, cultured in a medium supplemented with copper, become sensitized to polyphenol-induced growth inhibition.
"highlight2" >Dose?, apigenin at 5uM promoted growth in MCF10A cells and PC3 cancer cells. This could be because polyphenols at lower concentrations are known to be associated with cell proliferation [21], while behaving as prooxidants at high concentrations
"highlight2" >eff↓, Apigenin- and luteolin-induced antiproliferation and apoptosis in cancer cells is inhibited by cuprous chelator but not by iron and zinc chelators
"highlight2" >eff↓, EGCG and resveratrol, similar to that of the flavones luteolin and apigenin, also involves the mobilization of endogenous copper and consequent prooxidant effect leading to cell death.

1721- Lyco,  RES,  VitC,    Lycopene, resveratrol, vitamin C and FeSO4 increase damage produced by pro-oxidant carcinogen 4-nitroquinoline-1-oxide in Drosophila melanogaster: Xenobiotic metabolism implications.
- in-vitro, Pca, PC3 - in-vitro, Lung, A549 - in-vitro, Cerv, HeLa - in-vitro, BC, MCF-7 - in-vitro, Liver, HepG2
"highlight2" >ROS↑, We propose that the basal levels of the XM's enzymes in the ST cross interacted with a putative pro-oxidant activity of the compounds added to the pro-oxidant effects of 4-NQO.

873- QC,  RES,  CUR,  PI,    Combination Effects of Quercetin, Resveratrol and Curcumin on In Vitro Intestinal Absorption
- in-vitro, Nor, NA
"highlight2" >*BioEnh↑, Resveratrol received the greatest enhancement in permeability when combined with other agents: quercetin (310%), curcumin (300%), quercetin and curcumin (323%, 350% with piperine)

67- QC,  RES,    Overexpression of c-Jun induced by quercetin and resverol inhibits the expression and function of the androgen receptor in human prostate cancer cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, LAPC-4
"highlight2" >cJun↑,
"highlight2" >AR↓,
"highlight2" >NA↓,

3077- RES,    Resveratrol attenuates matrix metalloproteinase-9 and -2-regulated differentiation of HTB94 chondrosarcoma cells through the p38 kinase and JNK pathways
- in-vitro, Chon, HTB94
"highlight2" >MMP2↓, We found that resveratrol significantly inhibited MMP-2 and MMP-9, and induced the expression of type II collagen and sex-determining region Y-box (SOX)-9 and the production of sulfated proteoglycans in HTB94 chondrosarcoma cells.
"highlight2" >MMP9↓,
"highlight2" >SOX9↑,
"highlight2" >MMPs↓,
"highlight2" >p‑p38↑, Phosphorylation of p38 was increased and phosphorylation of c-Jun N-terminal kinase (JNK) was inhibited by resveratrol
"highlight2" >p‑JNK↓,
"highlight2" >NF-kB↓, Moreover, resveratrol reduced lung adenocarcinoma cell metastasis by suppressing heme oxygenase (HO)-1-mediated nuclear factor (NF)-κB pathway activation and subsequently downregulated the expression of MMPs.
"highlight2" >HO-1↓, Resveratrol inhibited the transcription-activator function of HO-1 and subsequently MMP-2 and MMP-9 expression in human lung cancer cells as well.

3065- RES,    Resveratrol-induced cytotoxicity in human Burkitt's lymphoma cells is coupled to the unfolded protein response
- in-vitro, lymphoma, NA
"highlight2" >UPR↑, treatment with RES lead to the activation of all 3 branches of the UPR
"highlight2" >IRE1↑, with early splicing of XBP-1 indicative of IRE1 activation, phosphorylation of eIF2α consistent with ER resident kinase (PERK) activation, activating transcription factor 6 (ATF6) splicing
"highlight2" >p‑eIF2α↑,
"highlight2" >PERK↑,
"highlight2" >ATF6↑,
"highlight2" >GRP78/BiP↑, increase in expression levels of the downstream molecules GRP78/BiP, GRP94 and CHOP/GADD153 in human Burkitt's lymphoma Raji and Daudi cell lines.
"highlight2" >GRP94↑,
"highlight2" >CHOP↑,
"highlight2" >GADD34↑, RES induces a pathway initiated by phosphorylation of eIF2α and followed by the upregulation of GADD34 and ATF4.
"highlight2" >ATF4↑,
"highlight2" >XBP-1↑, RES increased XBP-1 expression both in Raji and in Daudi cells
"highlight2" >Ca+2↑, RES was found to significantly increase cytosolic Ca2+
"highlight2" >ER Stress↑, RES was able to induce ER stress and activated all 3 branches of the UPR.

3078- RES,    The Effects of Resveratrol on Prostate Cancer through Targeting the Tumor Microenvironment
- Review, Pca, NA
"highlight2" >*ROS↓, RSV appears to be both pro- and anti-oxidant, depending on the circumstances [76]. In non-cancer tissues, RSV serves as an antioxidant [77], and therefore RSV can exert a beneficial effect on a wide variety of issues, including neuronal [78], anti-in
"highlight2" >ROS↑, However, to cancer cells with low pH environments due to the Warburg Effect, RSV shows more pro-oxidant characteristics.
"highlight2" >DNAdam↑, RSV can induce cancer cell death by inducing ROS accumulation, which subsequently leads to oxidative DNA damage and apoptosis
"highlight2" >Apoptosis↑,
"highlight2" >Hif1a↑, Wang et al. demonstrated that RSV-enhanced cancer cell death is due to the upregulation of HIF1α, which enhances ROS concentration in the TME beyond the limit for survival
"highlight2" >Casp3↑, superoxide can activate caspases 9 and 3, and subsequently promote the release of cytochrome C
"highlight2" >Casp9↑,
"highlight2" >Cyt‑c↑,
"highlight2" >Dose↝, It is important to note that low concentration of RSV can serve as a pro-oxidant that favors cell survival, and pro-apoptotic effects occur only at relatively higher RSV concentrations to stimulate superoxide production.
"highlight2" >MMPs↓, inhibitory effect of RSV on MMPs has been shown in many cancer types, and RSV is capable of inhibiting both MMP-2 and MMP-9
"highlight2" >MMP2↓,
"highlight2" >MMP9↓,
"highlight2" >EMT↓, RSV can restore the epithelial phenotype of the mesenchymal cells and inhibit the expression of EMT-related markers
"highlight2" >E-cadherin↑, RSV can inhibit EMT by up- and downregulating E-cadherin and N-cadherin, respectively, in prostate cancer cells.
"highlight2" >N-cadherin↓,
"highlight2" >AR↓, RSV can repress AR function by inhibiting AR transcriptional activity

3079- RES,    Therapeutic role of resveratrol against hepatocellular carcinoma: A review on its molecular mechanisms of action
- Review, Var, NA
"highlight2" >angioG↓, Resveratrol suppresses angiogenesis and metastatic markers to reverse cancer spread.
"highlight2" >TumMeta↓,
"highlight2" >ChemoSen↑, Resveratrol chemosensitizes chemotherapy and synergizes anti-cancer phytochemicals.
"highlight2" >NADPH↑, Both in vitro and in vivo studies indicates that resveratrol enhances various redox enzymes activity, especially nicotinamide adenine dinucleotide phosphate (NADPH)
"highlight2" >SIRT1↑, resveratrol effectively modulates both the cytokine and chemokine profiles in immune and endothelial cells by the upregulation of sirtuin-1 (SIRT1)
"highlight2" >NF-kB↓, suppression of NF-κB and prevention of the activation of NOD-like receptor family (Nrf) pyrin domain containing-3 inflammasome [
"highlight2" >NLRP3↓,
"highlight2" >Dose↝, The optimal dose of resveratrol being around 150 mg per day is considered safe by all means.
"highlight2" >COX2↓, Cox2 ↓; MMP9 ↓
"highlight2" >MMP9↓,
"highlight2" >PGE2↓, Cox1 and 2; PGE2↓
"highlight2" >TIMP1↑, Resveratrol suppresses the PMA-induced MMP activity in HepG2 cell line, while it also upregulates tissue inhibitor proteins of MMP, namely, TIMP1 and TIMP2, in dose-dependent manner
"highlight2" >TIMP2↑,
"highlight2" >Sp1/3/4↓, Resveratrol mitigates the expression of SP-1 by inhibiting both phosphorylation of JNK1/2 and expression of urokinase-type plasminogen activator in Huh-7 cell line
"highlight2" >p‑JNK↓,
"highlight2" >uPAR↓,
"highlight2" >ROS↓, Resveratrol attenuates the excessive ROS production and inflammatory cytokine, IL-6, and CXCR4 receptor expression by downregulating Gli-1 expression.
"highlight2" >CXCR4↓,
"highlight2" >IL6↓,
"highlight2" >Gli1↓,
"highlight2" >*ROS↓, redox imbalance may be attenuated by resveratrol via downregulating ROS production and simultaneously inducing antioxidant enzymes, GST, SOD, CAT and GPx activities in the cells
"highlight2" >*GSTs↑,
"highlight2" >*SOD↑,
"highlight2" >*Catalase↑,
"highlight2" >*GPx↑,
"highlight2" >*lipid-P↓, [72] observed that resveratrol treatment not only reduces lipid peroxidation but also increases GSH and GST serum levels in CCl4-treated rats as compared to the CCl4-control animals
"highlight2" >*GSH↑,
"highlight2" >eff↑, Resveratrol, in combination with thymoquinone (TQ), has been demonstrated to provide a synergistic antiproliferative efficacy against HCC cell lines as reported by Ismail et al.
"highlight2" >eff↑, Curcumin, a potential anticancer phytochemical, in combination with resveratrol has been reported to trigger synergistic apoptotic effects against Hepa1–6 cells
"highlight2" >eff↑, berberine in combination with resveratrol lowers the cell viability and cell adhesion. At low concentration, berberine significantly induces cell death while resveratrol inhibits cell migration in HepG2 cells

3076- RES,    Resveratrol for targeting the tumor microenvironment and its interactions with cancer cells
- Review, Var, NA
"highlight2" >IL6↓, A dose-dependent reduction of IL-6 by resveratrol led to attenuation of matrix metalloproteinases (MMPs), including MMP2 and MMP9
"highlight2" >MMPs↓,
"highlight2" >MMP2↓,
"highlight2" >MMP9↓,
"highlight2" >BioAv↓, The most important weakness of the usual form of resveratrol is its low absorption in the intestine and its low bioavailability
"highlight2" >Half-Life↑, some covers such as liposomes and micelles also can facilitate absorption and increase half-life
"highlight2" >BioAv↑, another study showed that carboxymethyl chitosan can increase bioavailability by more than 3.5 times
"highlight2" >Dose↝, low concentrations of resveratrol (lower than 50 uM) cause no remarkable toxicity for normal cells, while higher concentrations are associated with increased oxidative injury
"highlight2" >angioG↓, It is suggested that inhibition of STAT3, IL-10, and a reduction of vascular endothelial growth factor (VEGF) by resveratrol is involved in the suppression of macrophages and reduction of invasion and angiogenesis
"highlight2" >IL10↓,
"highlight2" >VEGF↓,
"highlight2" >NF-kB↓, Inhibition of NF-kB by resveratrol can attenuate the expression of COX-2.
"highlight2" >COX2↓,
"highlight2" >SIRT1↑, Activation of Sirt-1 by resveratrol has a role in the suppression of NF-kB
"highlight2" >Wnt↓, Resveratrol has also been shown that inhibit the Wnt/C-Myc pathway too
"highlight2" >cMyc↓,
"highlight2" >STAT3↓, Resveratrol has been shown that attenuate the expression of STAT3 through reduction of IL-6 level
"highlight2" >PTEN↑, Downregulation of miR-17, miR-20a and miR-106b by resveratrol can activate PTEN, which leads to suppression of PI3K and induction of apoptosis in cancer cells
"highlight2" >ROS↑, Resveratrol can trigger NOX5-induced ROS, leading to the induction of DNA damage and cancer cells senescence
"highlight2" >RadioS↑, The combination of radiation and resveratrol has shown that has a synergic effect for stimulation of ROS production and induction of senescence in non-small cell lung carci- noma
"highlight2" >Hif1a↓, Resveratrol can inhibit HIF-1α and its downstream proteins, including E-cadherin and vimentin
"highlight2" >E-cadherin↓,
"highlight2" >Vim↓,
"highlight2" >angioG↓, Furthermore, resveratrol inhibits angiogenesis markers and tumor growth through the inhibition of HIF-1a

3075- RES,  Rad,    The Protection Effect of Resveratrol Against Radiation-Induced Inflammatory Bowel Disease via NLRP-3 Inflammasome Repression in Mice
- in-vivo, Nor, NA
"highlight2" >*SIRT1↑, Here we show that resveratrol, the activator of Sirt1, could alleviate the bowel inflammation induced by irradiation and the expression of Sirt1 is consistent with the inflammation level.
"highlight2" >*radioP↑,
"highlight2" >*NLRP3↓, against radiation-induced inflammatory bowel disease via NLRP-3 inflammasome repression in mice and supports Sirt1 as a potential biomarker
"highlight2" >*Weight↑, The weight of C57BL / 6 mice in each group treated with resveratrol gradually increased from the 6th day after irradiation, while the weight of C57BL/6 mice in the irradiation group still showed a downward trend.
"highlight2" >*IL1β↓, Resveratrol Inhibited the Expression of IL-1β and NLRP-3 in Spleen and Thymus

3080- RES,    Resveratrol: A miraculous natural compound for diseases treatment
- Review, Var, NA
"highlight2" >SIRT1↑, PC12 cells Aβ‐induced apoptosis Inline graphic Feng et al. (2013) SIRT‐1↑ ROCK1↓
"highlight2" >ROCK1↓,
"highlight2" >AMPK↑, SAMP8 mice SIRT‐1 and AMPK↑
"highlight2" >*lipid-P↓, Sprague–Dawley rats Lipid peroxidation↓ Aβ aggregation in hippocampus↓
"highlight2" >Aβ↓,
"highlight2" >COX2↓, RSV decreases the prostaglandins (PGs) expression by inhibition of COX‐2 enzyme
"highlight2" >angioG↓, suggest that RSV may act as an anticancer agent to inhibit angiogenesis through affecting hypoxia‐inducible factor‐1 alpha (HIF‐1α) and vascular endothelial growth factor (VEGF) in different cancer cells in vitro
"highlight2" >Hif1a↓,
"highlight2" >VEGF↓,

3074- RES,    Possible therapeutic targets for NLRP3 inflammasome-induced breast cancer
- Review, BC, NA
"highlight2" >NLRP3↓, The active form of Resveratrol (RSV) inhibits NLRP3-mediated inflammasome activation by Sirt1 (SIRT1) / p53-dependent cellular aging.
"highlight2" >SIRT1↑,

3073- RES,    Resveratrol inhibits NLRP3 inflammasome activation by preserving mitochondrial integrity and augmenting autophagy
- in-vitro, Nor, NA
"highlight2" >*NLRP3↓, inhibits NLRP3 inflammasome-derived IL-1β secretion and pyroptosis in macrophages.
"highlight2" >*mtDam↓, Resveratrol inhibits the activation step of the NLRP3 inflammasome by suppressing mitochondrial damage
"highlight2" >*p38↑, Resveratrol also induces autophagy by activating p38, and macrophages treated with an autophagy inhibitor are resistant to the suppressive effects of resveratrol.

3072- RES,    Resveratrol ameliorates glioblastoma inflammatory response by reducing NLRP3 inflammasome activation through inhibition of the JAK2/STAT3 pathway
- in-vitro, GBM, LN229 - in-vitro, GBM, U87MG
"highlight2" >tumCV↓, RSV significantly inhibited cell viability in GBM cell lines LN-229 and U87-MG.
"highlight2" >TumCP↓, it inhibited the proliferation and invasive migration ability of GBM cells, while promoting apoptosis.
"highlight2" >TumCMig↓,
"highlight2" >Apoptosis↑,
"highlight2" >NLRP3↓, RSV inhibited the over-activation of the inflammasome NLRP3 through the JAK2/STAT3 signaling pathway.
"highlight2" >JAK2↓, by inhibiting the activation of the JAK2/STAT3 signaling pathway.
"highlight2" >STAT3↓,
"highlight2" >IL1β↓, RSV indeed decreased the levels of inflammasome NLRP3 and its downstream IL-1β, IL-18, IL-6, and TNFα.
"highlight2" >IL18↓,
"highlight2" >IL6↓,
"highlight2" >TNF-α↓,
"highlight2" >Inflam↓, partly mediated by improving the inflammatory state of GBM

3071- RES,    Resveratrol and Its Anticancer Effects
- Review, Var, NA
"highlight2" >chemoP↑, In this review, the effects of resveratrol are emphasized on chemopreventive, therapeutic, and anticancer.
"highlight2" >SIRT1↑, RSV can directly activate Sirt1 expression and induce autophagy independently or dependently on the mammalian target of rapamycin (mTOR)
"highlight2" >Hif1a↓, RSV suppresses tumor angiogenesis by inhibiting HIF-1a and VEGF protein
"highlight2" >VEGF↓,
"highlight2" >STAT3↓, RSV effectively prevents cancer by inhibiting STAT3 expression
"highlight2" >NF-kB↓, also has an inhibitory effect on antiapoptotic mediators such as NF-kB, COX-2, phosphatidylinositol 3-kinase (PI3K), and mTOR (52).
"highlight2" >COX2↓,
"highlight2" >PI3K↓,
"highlight2" >mTOR↓,
"highlight2" >NRF2↑, Activation of the Nrf2/antioxidant response element (ARE) pathway by endogenous or exogenous stimuli under normal physiological conditions has the potential to inhibit cancer and/or cancer cell survival, growth, and proliferation
"highlight2" >NLRP3↓, RSV downregulates the NLRP3 gene by activating the Sirt1 protein, thereby inducing autophagy
"highlight2" >H2O2↑, RSV mediates cytotoxicity in cancer cells by increasing intracellular hydrogen peroxide (H2O2) and oxidative stress levels that will cause cell death
"highlight2" >ROS↑,
"highlight2" >P53↑, RSV activates p53, increases the expression of PUMA and BAX
"highlight2" >PUMA↑,
"highlight2" >BAX↑,

3081- RES,    Resveratrol and p53: How are they involved in CRC plasticity and apoptosis?
- Review, CRC, NA
"highlight2" >NF-kB↓, At 5 µM, resveratrol repressed inflammation (NF-κB), CRC progression (FAK, Ki-67, MMP-9, CXCR4) and CSC production (CD44, CD133, ALDH1).
"highlight2" >FAK↓, Inhibition of FAK signaling pathway and thereby attenuation of invasion by resveratrol
"highlight2" >Ki-67↓,
"highlight2" >MMP9↓,
"highlight2" >CSCs↓,
"highlight2" >CD44↓,
"highlight2" >CD133↓,
"highlight2" >ALDH1A1↓,
"highlight2" >EMT↓, resveratrol inhibits not only EMT but also enhances CRC cells‘ sensitivity to the standard chemotherapeutic drug 5-FU
"highlight2" >ChemoSen↑,
"highlight2" >Hif1a↓, Suppression of HIF-1α using β1-integrin receptors through resveratrol, thereby inhibition of inflammation
"highlight2" >ITGB1↓,
"highlight2" >Inflam↓,

3070- RES,    Resveratrol inhibits tumor progression by down-regulation of NLRP3 in renal cell carcinoma
- in-vitro, RCC, ACHN - in-vitro, RCC, 786-O - in-vivo, NA, NA
"highlight2" >TumCP↓, We found that RSV inhibited tumor cells proliferation, migration and invasion and increased apoptosis of RCC either in vivo or in vitro.
"highlight2" >TumCMig↓,
"highlight2" >TumCI↓,
"highlight2" >Apoptosis↑,
"highlight2" >NLRP3↓, RSV significantly down-regulated expressions of NLRP3 and its downstream genes.

3082- RES,    Resveratrol Ameliorates the Malignant Progression of Pancreatic Cancer by Inhibiting Hypoxia-induced Pancreatic Stellate Cell Activation
- in-vitro, PC, PANC1 - in-vitro, PC, MIA PaCa-2 - in-vivo, NA, NA
"highlight2" >VEGF↓, Furthermore, our in vivo studies revealed that the administration of RSV to LSL-KrasG12D/+, Trp53fl/+, and Pdx1-Cre (KPC) mice by gastric perfusion could significantly suppress VEGF-A, SDF-1, IL-6, alpha-smooth muscle actin (α-SMA), and HIF-1α expres
"highlight2" >CXCL12↓,
"highlight2" >IL6↓,
"highlight2" >α-SMA↓,
"highlight2" >Hif1a↓,
"highlight2" >TumCI↓, RSV Suppresses Pancreatic Cancer Cell Invasion and EMT Induced by Hypoxia
"highlight2" >EMT↓,

3061- RES,    The Anticancer Effects of Resveratrol: Modulation of Transcription Factors
- Review, Var, NA
"highlight2" >AhR↓, Several reports demonstrate the inhibitory effects of resveratrol on AhR-mediated activation of phase I enzymes.
"highlight2" >NRF2↑, Bishayee et al. (18) demonstrated that attenuation of DENA (diethyl nitrosamine)-induced liver carcinogenesis by resveratrol was mediated by increased Nrf2 expression.
"highlight2" >*NQO1↑, Induction of Nrf2 signaling by resveratrol resulted in increased expression of NQO1, heme-oxygenase 1 (HO-1), and glutamate cysteine ligase catalytic subunit in cigarette smoke extract-treated bronchial epithelial cells
"highlight2" >*HO-1↑,
"highlight2" >*GSH↑, observed restored glutathione levels in cigarette smoke extract-treated A549 lung alveolar epithelial cancer cells by resveratrol;
"highlight2" >P53↑, we highlight reported resveratrol-induced, p53-mediated anticancer mechanisms.
"highlight2" >Cyt‑c↑, release of mitochondria proteins (e.g. cytochrome c, Smac/DIABLO, etc.) to the cytosol, thus triggering suppression of inhibitors of apoptosis proteins (e.g. Bcl2, Bcl-XL, survivin, XIAP, etc.) and caspase activation in several cancers
"highlight2" >Diablo↑,
"highlight2" >Bcl-2↓,
"highlight2" >Bcl-xL↓,
"highlight2" >survivin↓,
"highlight2" >XIAP↓,
"highlight2" >FOXO↑, activation of FoxO transcription factors is implicated in the observed anticancer activities of resveratrol.
"highlight2" >p‑PI3K↓, resveratrol's ability to inhibit the phosphorylation of PI3K/Akt (
"highlight2" >p‑Akt↓,
"highlight2" >BIM↑, Bim/TRAIL/DR4/DR5/p27KIP1 induction and cyclin D1 inhibition) of resveratrol on prostate cancer cells
"highlight2" >DR4↑,
"highlight2" >DR5↑,
"highlight2" >p27↑,
"highlight2" >cycD1↓,
"highlight2" >SIRT1↑, resveratrol is considered a SIRT1 agonist
"highlight2" >NF-kB↓, resveratrol not only curbs expression of NF-κB, but also impedes the phosphorylation of IκBα thereby keeping the constitutive NF-κB subunit in an inactive state, resulting in suppression of the inflammatory
"highlight2" >ATF3↑, Furthermore, increased ATF3 expression by resveratrol facilitated induction of apoptosis

3053- RES,    Resveratrol represses estrogen-induced mammary carcinogenesis through NRF2-UGT1A8-estrogen metabolic axis activation
- in-vitro, NA, NA
"highlight2" >NRF2↑, whereas treatment with resveratrol could upregulate the expression of NRF2 and UGT1A8, accelerate metabolic elimination of catechol estrogens, inhibit estrogen-induced DNA damage and suppress the pathological development of breast cancer.
"highlight2" >DNAdam↓, esveratrol attenuates mammary carcinogenesis through inhibiting estrogen-induced DNA damage

3054- RES,    Resveratrol induced reactive oxygen species and endoplasmic reticulum stress-mediated apoptosis, and cell cycle arrest in the A375SM malignant melanoma cell line
- in-vitro, Melanoma, A375
"highlight2" >TumCG↓, Treating A375SM cells with resveratrol resulted in a decrease in cell growth.
"highlight2" >P21↑, resveratrol was observed to increase the gene expression levels of p21 and p27, as well as decrease the gene expression of cyclin B.
"highlight2" >p27↑,
"highlight2" >CycB↓,
"highlight2" >ROS↑, generation of reactive oxygen species (ROS) and endoplasmic reticulum (ER) stress were confirmed at the cellular and protein levels
"highlight2" >ER Stress↑,
"highlight2" >p‑p38↑, Resveratrol induced the ROS-p38-p53 pathway by increasing the gene expression of phosphorylated p38 mitogen-activated protein kinase
"highlight2" >P53↑, while it induced the p53 and ER stress pathway by increasing the gene expression levels of phosphorylated eukaryotic initiation factor 2α and C/EBP homologous protein.
"highlight2" >p‑eIF2α↑,
"highlight2" >EP4↑,
"highlight2" >CHOP↑,
"highlight2" >Bcl-2↓, downregulating B-cell lymphoma-2 (Bcl-2) expression and upregulating Bcl-2-associated X protein expression
"highlight2" >BAX↓,
"highlight2" >TumCCA↑, Resveratrol induced cell cycle arrest of melanoma cell line
"highlight2" >NRF2↓, the decrease in Nrf2 expression caused by resveratrol may prevent the development of such resistance and thereby increase the sensitivity of melanoma cells to chemotherapy.
"highlight2" >ChemoSen↑,
"highlight2" >GSH↓, (GSH/GSSG) ratio was not measured, it can easily be assumed that the increased ROS generation by resveratrol reduced the GSH/GSSG ratio compared with the control

3055- RES,    Resveratrol and Tumor Microenvironment: Mechanistic Basis and Therapeutic Targets
- Review, Var, NA
"highlight2" >BioAv↓, Resveratrol is poorly bioavailable, and that considered the major hindrance to exert its therapeutic effect, especially for cancer management
"highlight2" >BioAv↓, at lower doses (25 mg per healthy subject) demonstrate that the mean proportion of free resveratrol in plasma was 1.7–1.9% with a mean plasma concentration of free resveratrol around 20 nM
"highlight2" >Dose↑, Boocock and his colleagues studied the pharmacokinetic of resveratrol; in vitro data showed that minimum of 5 µmol/L resveratrol is essential for the chemopreventive effects to be elicited
"highlight2" >eff↑, Despite the low bioavailability of resveratrol, it shows efficacy in vivo. This may be due to the conversion of both glucuronides and sulfate back to resveratrol in target organs such as the liver
"highlight2" >eff↑, repeated administration of high doses of resveratrol generates a higher plasma concentration of parent and a much higher concentration of sulfate and glucuronide conjugates in the plasma
"highlight2" >Dose↑, The doses tested in this study were 0.5, 1.0, 2.5 or 5.0 g daily for 29 days. No toxicity was detected, but moderate gastrointestinal symptoms were reported for 2.5 and 5.0 g doses
"highlight2" >BioAv↑, the co-administration of piperine with resveratrol was used to enhance resveratrol bioavailability
"highlight2" >ROS↑, Recent studies have shown that resveratrol increases ROS generation and decreases mitochondrial membrane potential
"highlight2" >MMP↓,
"highlight2" >P21↑, treatment decreased the viability of melanoma cells by activating the expression of both p21 and p27, which promoted cell cycle arrest.
"highlight2" >p27↑,
"highlight2" >TumCCA↑,
"highlight2" >ChemoSen↑, Additionally, the use of resveratrol with cisplatin in malignant human mesothelioma cells (MSTO-211H and H-2452 cells) synergistically induces cell death by increasing the intracellular ROS level [64].
"highlight2" >COX2↓, covers the down-regulation of the products of the following genes, COX-2, 5-LOX, VEGF, IL-1, IL-6, IL-8, AR and PSA [93].
"highlight2" >5LO↓,
"highlight2" >VEGF↓,
"highlight2" >IL1↓,
"highlight2" >IL6↓,
"highlight2" >IL8↓,
"highlight2" >AR↓,
"highlight2" >PSA↓,
"highlight2" >MAPK↓, by preventing also the activation of the MAPK and PI3K/Akt signaling pathways, it suppresses HIF-1a and VEGF release in ovarian cancer cells of humans
"highlight2" >Hif1a↓,
"highlight2" >Glycolysis↓, Resveratrol was found to effectively impede the activation, invasion, migration and glycolysis of PSCs induced by reactive oxygen species (ROS) by down-regulating the expression of microRNA 21 (miR-21)
"highlight2" >miR-21↓,
"highlight2" >PTEN↑, also by increasing the phosphatise and tensin homolog (PTEN) protein levels
"highlight2" >Half-Life↝, 25 mg/70 kg resveratrol administered to healthy human participants, the compound predominantly appeared in the form of glucuronide and sulfate conjugates in serum and urine and reached its peak concentrations in serum about 30 min after ingestion
"highlight2" >*IGF-1↓, Brown and colleagues noted how a major decline in circulating insulin-like growth factor (IGF)-I as well as IGF-binding proteins (IGFBP-3) among healthy individuals can be credited to the intake of resveratrol
"highlight2" >*IGFBP3↑,
"highlight2" >Half-Life↓, Microactive® and Resveratrol SR and manufactured by Bioactives. This compound is capable of sustained release for over 12 h to increase intestinal residence time.

3056- RES,    Less is more for cancer chemoprevention: evidence of a non-linear dose response for the protective effects of resveratrol in humans and mice
- in-vivo, Nor, NA
"highlight2" >*AMPK↑, Efficacy correlated with increased AMP-activated protein kinase (AMPK) activation and the senescence marker p21.
"highlight2" >*P21↑,
"highlight2" >*Dose↓, Our results show that low dietary exposures not only elicit biological changes in mouse and human tissues relevant to colorectal cancer chemoprevention, but they have superior efficacy compared to high doses
"highlight2" >*chemoP↑, Superior cancer chemopreventive efficacy of low dose resveratrol

3057- RES,    The therapeutic effect of resveratrol: Focusing on the Nrf2 signaling pathway
- Review, Var, NA - Review, AD, NA - Review, Stroke, NA
"highlight2" >*NRF2↑, Resveratrol stimulates the Nrf2 signaling through blockage of Keap1
"highlight2" >*Keap1↓,
"highlight2" >*ROS↓, Res ameliorates oxidative stress, apotosis and inflammatory indexes in several tissues.
"highlight2" >*Apoptosis↓,
"highlight2" >*Inflam↓,
"highlight2" >*antiOx↑, Beneficial effects such as anti-inflammatory, antioxidant, hepatoprotective, neuroprotective, cardioprotective, renoprotective, anti-obesity, anti-diabetic, and anti-cancer
"highlight2" >*hepatoP↑,
"highlight2" >*neuroP↑, neuroprotective Res-associated effect resulting in the activation of Nrf2 signaling pathway.
"highlight2" >*cardioP↑,
"highlight2" >*RenoP↑,
"highlight2" >*AntiCan↑,
"highlight2" >*memory↑, Res could ameliorate the spatial memory in the experimental animals via increasing the SOD, glutathione peroxidase (GPx) and CAT expression and activity.
"highlight2" >*SOD↑,
"highlight2" >*GPx↑,
"highlight2" >*Catalase↑,
"highlight2" >*MDA↓, Res decreased malondialdehyde (MDA) brain levels in these mice activating the Nrf2/HO-1, indicating its potential to decrease the cell oxidative damage.
"highlight2" >*NRF2↑,
"highlight2" >*HO-1↑,
"highlight2" >*ROS↓,
"highlight2" >*Aβ↓, Res improved AD by reducing Aβ protein expression in the brain of treated mice
"highlight2" >*iNOS↓, Res ameliorated Aβ-induced increase of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2)(pro-inflammatory enzymes), reversed and decreased the mRNA expression levels of antioxidative genes (GPx1, SOD-1, Nrf2, CAT, glutathione, and
"highlight2" >*COX2↓,
"highlight2" >*GSH↑, Res, significantly reduced NSCs death and the MDA levels, raising proliferation, SOD activity, and GSH content after OGD/R damage
"highlight2" >*HO-1⇅, through marked the Nrf2/HO-1 upregulation in hypoxia-ischemia pups
"highlight2" >*SIRT1↑, restored activity and expression of SIRT1 mediated by Nrf2.

3058- RES,    Resveratrol inhibits estrogen-induced breast carcinogenesis through induction of NRF2-mediated protective pathways
- in-vivo, NA, NA
"highlight2" >*Nrf1?, Resveratrol treatment alone or in combination with E2 significantly upregulated expression of nuclear factor erythroid 2-related factor 2 (NRF2) in mammary tissues.

3059- RES,    Resveratrol, an Nrf2 activator, ameliorates aging-related progressive renal injury
- in-vivo, Nor, HK-2
"highlight2" >*RenoP↑, Resveratrol improved renal function, proteinuria, histological changes and inflammation in aging mice
"highlight2" >*Inflam↓,
"highlight2" >*NRF2↑, expression of Nrf2-HO-1-NOQ-1 signaling and SIRT1-AMPK-PGC-1α signaling was increased in the RSV group
"highlight2" >*HO-1↑,
"highlight2" >*SIRT1↑,
"highlight2" >*ROS↓, Activation of the Nrf2 and SIRT1 signaling pathways ameliorated oxidative stress and mitochondrial dysfunction.
"highlight2" >AntiAge↑, Pharmacological targeting of Nrf2 signaling molecules may reduce the pathologic changes of aging in the kidney

3060- RES,    Resveratrol targeting NRF2 disrupts the binding between KEAP1 and NRF2-DLG motif to ameliorate oxidative stress damage in mice pulmonary infection
- in-vitro, Nor, RAW264.7 - in-vivo, NA, NA
"highlight2" >*NRF2↑, RES triggers the activation of NRF2, resulting in an anti-oxidative effect
"highlight2" >*antiOx↑,
"highlight2" >*ROS↓, RES ameliorates oxidative stress damage in the lung tissue of mice with pathogenic condition.

3069- RES,    Resveratrol Inhibits NLRP3 Inflammasome-Induced Pyroptosis and miR-155 Expression in Microglia Through Sirt1/AMPK Pathway
- in-vitro, Nor, N9
"highlight2" >*antiOx↑, antioxidant, anti-carcinogenic, anti-obesity, anti-aging, anti-inflammatory, immunomodulatory properties.
"highlight2" >*Inflam↓,
"highlight2" >*ROS↓, Our results demonstrated that resveratrol inhibits LPS- and ATP-activated NLRP3 inflammasome and protects microglial cells upon oxidative stress, proinflammatory cytokine production, and pyroptotic cell death resulting from inflammasome activation.
"highlight2" >*NF-kB↓, resveratrol inhibits nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling and activates AMPK/Sirt1 pathways.
"highlight2" >*AMPK↑,
"highlight2" >*SIRT1↑,
"highlight2" >*miR-155↓, Furthermore, our results indicated that resveratrol downregulated inflammasome-induced miR-155 expression
"highlight2" >*NLRP3↓, To sum up, our results suggest that resveratrol suppresses the NLRP3 inflammasome and miR-155 expression through AMPK and Sirt1 pathways in microglia.

3062- RES,    Resveratrol enhances post-injury muscle regeneration by regulating antioxidant and mitochondrial biogenesis
- in-vivo, Nor, NA
"highlight2" >*antiOx↑, RES enhanced antioxidant capacity via the Kelch-like ECH-associated protein 1 (KEAP-1)/nuclear factor erythroid 2-related factor 2 (NRF2)/heme oxygenase-1 (HO-1) signaling pathway
"highlight2" >*Keap1↓,
"highlight2" >*NRF2↑,
"highlight2" >*HO-1↑,
"highlight2" >*GPx↑, as indicated by elevated activities of total antioxidant capacity, Glutathione peroxidase (GSH-PX), and superoxidase dismutase (SOD).
"highlight2" >*SOD↑,

3063- RES,    Resveratrol: A Review of Pre-clinical Studies for Human Cancer Prevention
- Review, Var, NA
"highlight2" >*Inflam↓, Resveratrol is known to have potent anti-inflammatory and anti-oxidant effects and to inhibit platelet aggregation and the growth of a variety of cancer cells.
"highlight2" >*antiOx↑,
"highlight2" >*AntiAg↑,
"highlight2" >*chemoP↑, Its potential chemopreventive and chemotherapeutic activities have been demonstrated in all three stages of carcinogenesis
"highlight2" >ChemoSen↑,
"highlight2" >BioAv↑, Compared to other known polyphenols, such as quercetin and catechin, trans-resveratrol is well absorbed much more efficiently following oral administration to humans
"highlight2" >Half-Life↝, Compared to resveratrol, which has a plasma half-life of 8–14 min, the metabolites have a plasma half-life of about 9.2 hours
"highlight2" >COX2↓, there was inhibited expression of anti-apoptotic proteins, such as survivin, and markers of tumor promotion, cyclooxygenase (COX)-2, and ornithine decarboxylase (ODC) were observed
"highlight2" >cycD1↓, Resveratrol decreased the expression of cyclins D1 and D2, Cdk 2, 4 and 6, and proliferating cell nuclear antigen (PCNA) whereas p21WAF1/CIP1 was increased
"highlight2" >CDK2↓,
"highlight2" >CDK4↓,
"highlight2" >CDK6↓,
"highlight2" >P21↑,
"highlight2" >MMP9↓, associated with decreased COX-2 and matrix metalloprotease-9 expression and suppression of NFκB activation
"highlight2" >NF-kB↓,
"highlight2" >Telomerase↓, Relatively high concentrations also substantially downregulate telomerase activity
"highlight2" >PSA↓, Resveratrol downregulates PSA by a mechanism independent of changes in AR
"highlight2" >MAPK↑, Resveratrol treatment of various prostate cells also accompanied the activation of MAPK signaling and an increase in cellular p53
"highlight2" >P53↑,

3064- RES,    Resveratrol Suppresses Cancer Cell Glucose Uptake by Targeting Reactive Oxygen Species–Mediated Hypoxia-Inducible Factor-1α Activation
- in-vitro, CRC, HT-29 - in-vitro, BC, T47D - in-vitro, Lung, LLC1
"highlight2" >FDG↓, Resveratrol mildly decreased cell content and more pronouncedly suppressed 18F-FDG uptake in Lewis lung carcinoma, HT-29 colon, and T47D breast cancer cells.
"highlight2" >ROS↓, Resveratrol also decreased intracellular ROS in patterns that closely paralleled 18F-FDG uptake.
"highlight2" >Hif1a↓, HIF-1α protein was markedly reduced by resveratrol,
"highlight2" >GLUT1↓, 50uM, Resveratrol Inhibits Glut-1 Expression and Lactate Production
"highlight2" >lactateProd↓,

3088- RES,    Notch signaling mediated repressive effects of resveratrol in inducing caspasedependent apoptosis in MCF-7 breast cancer cells
- in-vitro, BC, MCF-7
"highlight2" >NOTCH1↓, findings further displayed a significant reduction in cell viability in resveratrol-treated MCF-7 cancer cells, which were concomitantly related to the downregulation of Notch-1, Jagged-1, and DLL4.
"highlight2" >BAX↑, expression of Bax, Bcl-2, cyclin D1, CDK4, p21, and caspase-3 activation.
"highlight2" >CDK4↝,
"highlight2" >Casp3↑,
"highlight2" >P21↑,

3066- RES,    Resveratrol triggers ER stress-mediated apoptosis by disrupting N-linked glycosylation of proteins in ovarian cancer cells
"highlight2" >GSK‐3β↑, resveratrol suppressed the hexosamine biosynthetic pathway and interrupted protein glycosylation through GSK3β activation
"highlight2" >Akt↓, Akt attenuation in response to resveratrol.
"highlight2" >CHOP↑, Resveratrol-mediated disruption of protein glycosylation induced cellular apoptosis as indicated by the up-regulation of GADD153, followed by the activation of ER-stress sensors (PERK and ATF6α).
"highlight2" >ER Stress↑,
"highlight2" >PERK↑,
"highlight2" >ATF6↑,
"highlight2" >UPR↑, Disruption of protein glycosylation causes the accumulation of aberrant of proteins in the endoplasmic reticulum (ER) which in turn activates unfolded protein responses (UPR) in the ER, leading to severe stressful conditions
"highlight2" >GlucoseCon↓, Previous studies have shown that resveratrol (RSV) impairs glucose consumption via Akt/GLUT1 axis in cancer [

3067- RES,    Proteomic Profiling Reveals That Resveratrol Inhibits HSP27 Expression and Sensitizes Breast Cancer Cells to Doxorubicin Therapy
- in-vitro, BC, MCF-7
"highlight2" >Apoptosis↑, Consistently, we demonstrated that resveratrol induces apoptosis in MCF-7 cells
"highlight2" >MMP↓, Apoptosis was associated with a significant increase in mitochondrial permeability transition, cytochrome c release in cytoplasm, and caspases -3 and -9 independent cell death.
"highlight2" >Cyt‑c↑,
"highlight2" >Casp3↑,
"highlight2" >Casp9↑,
"highlight2" >HSP27↓, We propose that potential modulation of HSP27 levels using natural alternative agents, as resveratrol, may be an effective adjuvant in breast cancer therapy

3068- RES,    Resveratrol decreases the expression of genes involved in inflammation through transcriptional regulation
- in-vitro, lymphoma, U937
"highlight2" >p65↓, In our study, RESV treatment significantly decreased p65 expression and reduced the activities of the antioxidant enzymes SOD2, PRX2, CAT, and TRX.
"highlight2" >SOD2↓,
"highlight2" >Prx↓,
"highlight2" >Catalase↓,
"highlight2" >Trx↓,
"highlight2" >TNF-α↓, (i.e., TNF-α, IL-8, and MCP-1), whereas a reduction in the protein levels of these cytokines was observed in the presence of RESV.
"highlight2" >IL8↓,
"highlight2" >MCP1↓,
"highlight2" >SIRT1↑, a trend of increased SIRT1 activity in the presence of RESV was observed, which may be due to the low dose of RESV used

3099- RES,    Resveratrol and cognitive decline: a clinician perspective
- Review, Nor, NA - NA, AD, NA
"highlight2" >*antiOx↑, In preclinical models of cognitive decline, resveratrol displays potent antioxidant activity by scavenging free radicals, reducing quinone reductase 2 activity and upregulating endogenous enzymes.
"highlight2" >*ROS↓,
"highlight2" >*cognitive↑,
"highlight2" >*neuroP↑,
"highlight2" >*SIRT1↑, By inducing SIRT1, resveratrol may promote neurite outgrowth and enhance neural plasticity in the hippocampal region
"highlight2" >*AMPK↑, Resveratrol also induces neurogenesis and mitochondrial biogenesis by enhancing AMP-activated protein kinase (AMPK), which is known to stimulate neuronal differentiation and mitochondrial biogenesis in neurons.
"highlight2" >*GPx↑, figure 1
"highlight2" >*HO-1↑,
"highlight2" >*GSK‐3β↑,
"highlight2" >*COX2↓,
"highlight2" >*PGE2↓, Resveratrol also inhibits pro-inflammatory enzyme (i.e., COX-1 and -2) expression, reduces NF-κB activation as well as PGE2, NO, and TNF-α production, and cytokine release
"highlight2" >*NF-kB↓,
"highlight2" >*NO↓,
"highlight2" >*Casp3↓,
"highlight2" >*MMP3↓,
"highlight2" >*MMP9↓,
"highlight2" >*MMP↑, resveratrol attenuated ROS production and mitochondrial membrane-potential disruption; moreover, it restored the normal levels of glutathione (GSH) depleted by Aβ1-42
"highlight2" >*GSH↑,
"highlight2" >*other↑, resveratrol significantly increased cerebral blood flow (CBF) in the frontal cortex of young healthy humans.
"highlight2" >*BioAv↑, receiving 200 mg/day of resveratrol in a formulation with quercetin 320 mg [53], in order to increase its bioavailability,
"highlight2" >*memory↑, Resveratrol supplementation induced retention of memory and improved the functional connectivity between the hippocampus and frontal, parietal, and occipital areas, compared with placebo
"highlight2" >*GlutMet↑, Also, glucose metabolism was improved and this may account for some of the beneficial effects of resveratrol on neuronal function.
"highlight2" >*BioAv↓, The main problems related to the therapeutic or preventive use of resveratrol are linked to its low oral bioavailability and its short half-life in serum
"highlight2" >*Half-Life↓,
"highlight2" >*toxicity∅, On the other hand, the tolerability and safety profile of resveratrol is very high

4289- RES,    Resveratrol Attenuates Formaldehyde Induced Hyperphosphorylation of Tau Protein and Cytotoxicity in N2a Cells
- in-vitro, AD, NA
"highlight2" >*antiOx↑, Resveratrol (Res), as a polyphenol anti-oxidant, has been considered to have therapeutic potential for the treatment of AD.
"highlight2" >*p‑tau↓, Res significantly decreased FA-induced cytotoxicity, reduced cell apoptosis rates, and inhibited the hyperphosphorylation of tau protein at Thr181 in a dose-dependent manner.
"highlight2" >*GSK‐3β↓, Further tests revealed that this effect was associated with the suppression of glycogen synthase kinase (GSK-3β)
"highlight2" >*CaMKII ↓, and calmodulin-dependent protein kinase II (CaMKII) activities, both of which are important kinases for tau protein hyperphosphorylation.
"highlight2" >*PP2A↑, Res was found to increase the activity of phosphoseryl/phosphothreonyl protein phosphatase-2A (PP2A).
"highlight2" >*neuroP↑, Neuroprotective effects of Res against FA-induced cytotoxicity

4288- RES,    Trans-resveratrol Inhibits Tau Phosphorylation in the Brains of Control and Cadmium Chloride-Treated Rats by Activating PP2A and PI3K/Akt Induced-Inhibition of GSK3β
- in-vivo, AD, NA
"highlight2" >*memory↑, RES improved both short and long-term memory as analyzed by novel object recognition task and significantly increased brain levels of glutathione in both control and CdCl2-treated rats.
"highlight2" >*GSH↑,
"highlight2" >*ROS↓, It also inhibited ROS levels of malondialdehyde in the brains of CdCl2-treated rats.
"highlight2" >*MDA↓,
"highlight2" >*p‑tau↓, RES decreased the phosphorylation rate of Tau at Ser199 and Ser296.
"highlight2" >*PI3K↑, RES activated PI3K/Akt signaling pathway in both control and CdCl2 treated rats by increasing levels of p-PI3K (Tyr607) and p-Akt (Ser473)
"highlight2" >*Akt↑,
"highlight2" >*AMPK↑, significant increase in the levels of AMPK and p-AMPK, known upstream regulators of PI3K/Akt signaling pathway.
"highlight2" >*PP2A↑, RES inhibits Tau phosphorylation in rat’s brain by activating PP2A protein and AMPK/PI3K/Akt-induced inhibition of GSK3β.
"highlight2" >*GSK‐3β↓,

4287- RES,    Resveratrol targeting tau proteins, amyloid-beta aggregations, and their adverse effects: An updated review
- Review, AD, NA
"highlight2" >*p‑tau↓, Res supplementation is beneficial in dephosphorylation of tau proteins and suppressing their aggregations.

4286- RES,    Neuroprotective Properties of Resveratrol and Its Derivatives—Influence on Potential Mechanisms Leading to the Development of Alzheimer’s Disease
- Review, AD, NA
"highlight2" >*neuroP↑, state of the art evidence on the role of resveratrol (RSV) in neuroprotection is presented
"highlight2" >*Inflam↓, Resveratrol (3,5,4′-trihydroxy-trans-stilbene), a polyphenol contained in red wine, peanuts, and some berries, is known for its anti-atherosclerotic, anti-inflammatory, antioxidant, and longevity-promoting properties
"highlight2" >*antiOx↑,
"highlight2" >*GSH↑, ↑glutathione in brain
"highlight2" >*HO-1↑, ↑HO-1 ↓iNOS in hippocampus
"highlight2" >*iNOS↓,
"highlight2" >*BDNF↑, ↑BDNF, ↑pCREB, ↑PKA, ↑BCl-2 expression, ↓BAX expression, ↓IL-1β, IL-6, in hippocampus
"highlight2" >*p‑CREB↑,
"highlight2" >*PKA↑,
"highlight2" >*Bcl-2↑,
"highlight2" >*BAX↓,
"highlight2" >*IL1β↓,
"highlight2" >*IL6↓,
"highlight2" >*MMP9↓, ↓MMP-9 in cerebrospinal fluid
"highlight2" >*memory↑, ↑memory performance
"highlight2" >*AMPK↑, ↑AMPK, ↑PGC-1, ↓NF-κB / IL-1β / NLRP3 in hippocampus and prefrontal cortex
"highlight2" >*PGC-1α↓,
"highlight2" >*NF-kB↓,
"highlight2" >*Aβ↓, may counteract the formation of neurotoxic Aβ
"highlight2" >*SIRT1↑, Resveratrol via SIRT-1 can, therefore, be expected to reduce the level of hyperphosphorylated tau and provide protection against neurodegeneration.
"highlight2" >*p‑tau↓,
"highlight2" >*PP2A↑, resveratrol by lowering the expression of MID1 ubiquitin ligase increases protein phosphatase 2A (PP2A) activity and promotes tau dephosphorylation by preventing its accumulation
"highlight2" >*lipid-P↓, resveratrol abolishes Aβ-induced lipid peroxidation and expression of heme oxygenase-1 (HO-1) reduction;
"highlight2" >*NLRP3↓, Researchers achieved a significant reduction in the levels of NF-κB (nuclear factor κ-light-chain enhancer of activated B cell), interleukin 1β and NLRP3 (NOD-, LRR- and pyrin domain-containing protein 3) inflammation markers
"highlight2" >*BACE↓, figure 1

4285- RES,    Resveratrol Rescues Tau-Induced Cognitive Deficits and Neuropathology in a Mouse Model of Tauopathy
- in-vivo, AD, NA
"highlight2" >*tau↓, RSV significantly inhibited tau aggregation and tau oligomer-induced cytotoxicity, and blocked the uptake of extracellular tau oligomers by N2a cells
"highlight2" >*cognitive↑, RSV treatment effectively rescued cognitive deficits, reducing the levels of phosphorylated tau, neuroinflammation and synapse loss in the brains of mice.
"highlight2" >*Inflam↓,

4284- RES,    Resveratrol induces dephosphorylation of Tau by interfering with the MID1-PP2A complex
- in-vitro, AD, HEK293 - NA, Stroke, NA - in-vivo, AD, NA
"highlight2" >*p‑tau↓, Resveratrol induces dephosphorylation of Tau
"highlight2" >*PP2A↑, resveratrol, a polyphenol, significantly induces PP2A activity and reduces Tau phosphorylation at PP2A-dependent epitopes.
"highlight2" >*neuroP↑, resveratrol is more and more being established as a neuroprotective drug after ischemic brain injury and in neurodegenerative disorders including Parkinson’s Disease13,14, AD15,16 and Huntington’s Disease
"highlight2" >*antiOx↑, resveratrol has anti-oxidant activity19,20, inhibits cycloxygenase activity21,22, ribonucleotide reductase23, protein kinase C24, DNA polymerase 25 and has antiestrogenic properties26,27 and anti-platelet activity
"highlight2" >COX2↓,
"highlight2" >*AntiAg↑,
"highlight2" >*SIRT1↑, it activates Sirt1, an NAD+-dependent protein deacetylase28,29 and also has been demonstrated to activate AMP kinase (AMPK)30,31, an important glucose sensor that inhibits acetyl-CoA carboxylase, thereby increasing oxidation of fatty acids and decre
"highlight2" >*AMPK↑,
"highlight2" >*Acetyl-CoA↓,
"highlight2" >*FAO↑,
"highlight2" >*ADAM10↑, Resveratrol has been suggested to induce the α-secretase ADAM10, which outcompetes BACE1 and thereby reduces Aβ-production
"highlight2" >*BACE↓,
"highlight2" >*Aβ↓,
"highlight2" >*memory↑, interestingly, the resveratrol-mediated reduction of Aβ increases life span and improves learning and memory
"highlight2" >*Inflam↓, reduces neuroinflammation47 and reduces oxidative stress48.
"highlight2" >*ROS↓,

4154- RES,    Resveratrol improves postnatal hippocampal neurogenesis and brain derived neurotrophic factor in prenatally stressed rats
- in-vivo, AD, NA
"highlight2" >*neuroP↑, Resveratrol is known to exert its neuroprotective potential by enhancing neurogenesis.
"highlight2" >*BDNF↑, Resveratrol treatment has improved the expression of DCX +ve neurons and BDNF expression.

4153- RES,    Effect of oral resveratrol on the BDNF gene expression in the hippocampus of the rat brain
- in-vivo, AD, NA
"highlight2" >*neuroP↑, findings suggest that the neuroprotective effects of resveratrol may be at least partly due to its inducing effects on the expression levels of the BDNF mRNA.
"highlight2" >*BDNF↑,

3863- RES,  MEL,  VitA,RetA,    Target Enzymes Considered for the Treatment of Alzheimer's Disease and Parkinson's Disease
- Review, AD, NA - Review, Park, NA
"highlight2" >*ADAM10↑, resveratrol, with a polyphenol framework found in grape skin, peanut, and pomegranates, has been reported to be applied for the treatment of ND to enhance ADAM10 expression indirectly.
"highlight2" >*ADAM10↑, In short, ADAM10 activity could be elevated by biological molecules such as XBP-1, SOX-2, PAX2, and melatonin.
"highlight2" >*ADAM10↑, Small molecules such as bryostatin-1, retinoic acid, acitretin, Am80, and phlogacantholide C and multiple natural products (i.e., resveratrol, gemfibrozil, and etazolate) have been reported as upregulators of ADAM10.

3858- RES,    Alpha-Secretase ADAM10 Regulation: Insights into Alzheimer’s Disease Treatment
- Review, AD, NA
"highlight2" >*neuroP↑, exerts neuroprotective and antioxidant properties
"highlight2" >*antiOx↑,
"highlight2" >*LDL↓, RSV decreases total cholesterol concentration in hypercholesterolemic rats
"highlight2" >*ADAM10↑, RSV under experimental conditions in CHO (chinese hamster ovary) cells expressing human APP695 containing a Swedish mutation showed a significant increase in ADAM10 expression,

3798- RES,    Resveratrol reverses hippocampal synaptic markers injury and SIRT1 inhibition against developmental Pb exposure
- in-vivo, NA, NA
"highlight2" >*SIRT1↑, Resveratrol attenuated a decrease in the expression levels of SIRT1 and BDNF induced by Pb
"highlight2" >*BDNF↑,
"highlight2" >*PSD95↑, Moreover, resveratrol treatment reversed the decrease in PSD-95 and NL-1 expression induced by Pb.
"highlight2" >*memory↑, Resveratrol improved spatial learning and memory deficits in Pb- exposed rats

3614- RES,    Resveratrol--a boon for treating Alzheimer's disease?
- Review, AD, NA
"highlight2" >*SIRT1↑, resveratrol-induced SIRT1 was found to protect neurons
"highlight2" >*neuroP↑,

3613- RES,    Resveratrol for Alzheimer's disease
- Review, AD, NA
"highlight2" >*SIRT1↑, Resveratrol is a potent activator of SIRT1, and thus may mimic caloric restriction to prevent diseases of aging.
"highlight2" >*BioAv↝, Resveratrol (1) is detectable in cerebrospinal fluid (at low nanomolar levels),
"highlight2" >*toxicity↓, (2) is safe and well tolerated
"highlight2" >*ROS↓, Through SIRT1 activation, resveratrol may protect neurons from reactive oxygen species (ROS), hydrogen peroxide free radicals,
"highlight2" >*antiOx↑, Similarly, its antioxidant capabilities may decrease the generation of Aβ through inhibition of ROS-activated enzymes
"highlight2" >*Aβ↓,
"highlight2" >*MMP9↓, 50% decrease in CSF matrix metalloproteinase 9 (MMP-9) level with resveratrol
"highlight2" >*TNF-α↓, we found reduced plasma levels of the pro-inflammatory markers IL-1r4, IL-12P40, IL-12P70, and TNF-α in the treatment group

3612- RES,    Resveratrol in Alzheimer's disease: a review of pathophysiology and therapeutic potential
- Review, AD, NA
"highlight2" >*other↑, Resveratrol demonstrates beneficial and protective effects in AD models and seems to provide a promising therapeutic alternative.
"highlight2" >*Aβ↓, Disaggregation of Aβ-peptides
"highlight2" >*Inflam↓, Activated microglia seem to be an important target of the neuroprotective activity of resveratrol, resulting in the reduc- tion of pro-inflammatory factors 3
"highlight2" >*NF-kB↓, its ability to inhibit the NF-κB signaling pathway in activated microglia
"highlight2" >*neuroP↑, Neuroprotective effects were also observed with the injection of resveratrol in rats (100 μM/5 μL),
"highlight2" >*HO-1↑, which reduced amyloid accumulation, protected animals against neuronal death, increased antioxidant enzyme heme oxygenase-1 (HO-1) expression, and suppressed lipid peroxidation in the hippocampus.
"highlight2" >*lipid-P↓,
"highlight2" >*COX2↓, inhibiting the generation of TNF, APP, cyclooxygenase (COX)-2 and NF-κB phosphorylation in the hippocampus
"highlight2" >*AMPK↑, Resveratrol is a potent activator of AMPK, thereby implicating another pathway through that its neuroprotective effects may be exerted
"highlight2" >*Catalase↑, Resveratrol (10 μM) attenuated lipid peroxidation and upregulated antioxidant enzyme levels, such as catalase, superoxide dismutase (SOD), and glutathione reductase (GR).
"highlight2" >*SOD↑,
"highlight2" >*GSR↑,
"highlight2" >*ROS↓, administration of resveratrol (10 and 20 μM) reduced ROS production in cells treated with AGEs
"highlight2" >*MMP9↓, attenuated neuroinflammation, reduced proinflammatory markers, and decreased MMP-9 in the CSF
"highlight2" >*cognitive↑, Resveratrol also attenuated the patients’ cognitive and functional decline
"highlight2" >*SIRT1↑, neuroprotection is through the activation of the sirtuin 1 (SIRT1) pathway, which in turn inhibits the activation of the NF-κB signaling pathway.
"highlight2" >*IL1β↓, reducing Aβ-induced memory and learning impairment and decreasing the expression of proinflammatory cytokines (IL-1β and IL-6)
"highlight2" >*IL6↓,

3100- RES,    Neuroprotective effects of resveratrol in Alzheimer disease pathology
- Review, AD, NA
"highlight2" >*neuroP↑, several studies have reported interesting insights about the neuroprotective properties of the polyphenolic compound resveratrol
"highlight2" >*BioAv↓, However, resveratrol’s low bioavailability originating from its poor water solubility and resulting from its short biological half-life
"highlight2" >*Half-Life↓,
"highlight2" >*BioAv↑, encapsulation in liposomal formulations
"highlight2" >*BBB↑, Resveratrol being a lipophilic compound can readily cross the BBB via transmembrane diffusion
"highlight2" >*NRF2↑, resveratrol into aged cells leading to the activation of cellular Nrf2-mediated antioxidant defense systems
"highlight2" >*BioAv↓, An oral dose of 25 mg results in less than 5 μg/mL in the serum following absorption through the gastrointestinal tract, corresponding to approximately a 1000-fold decrease in bioavailability.
"highlight2" >*BioAv↑, Treatment with pterostilbene also produced a sevenfold rise in its oral bioavailability than the parent resveratrol
"highlight2" >*SIRT1↑, Amongst all the naturally occurring activators of SIRT 1, resveratrol is considered to be the most effective SIRT 1 activator.
"highlight2" >*cognitive↑, Pterostilbene has shown to be a potent modulator of cognition and cellular oxidative stress associated with AD
"highlight2" >*lipid-P↓, Figure 2
"highlight2" >*HO-1↑,
"highlight2" >*SOD↑,
"highlight2" >*GSH↑,
"highlight2" >*GPx↑,
"highlight2" >*G6PD↑,
"highlight2" >*PPARγ↑,
"highlight2" >*AMPK↑,
"highlight2" >*Aβ↓, Lowered Aβ levels by activating AMPK pathway

3083- RES,    Resveratrol suppresses breast cancer cell invasion by inactivating a RhoA/YAP signaling axis
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MDA-MB-468
"highlight2" >YAP/TEAD↓, we demonstrate that resveratrol decreases the expression of YAP target genes
"highlight2" >Rho↓, Strikingly, we also demonstrate that resveratrol inactivates RhoA, leading to the activation of Lats1 and induction of YAP phosphorylation.
"highlight2" >FAK↓, REV decreases breast cancer cell invasion by inhibiting FAK,44 Rac and Cdc4245 activities
"highlight2" >MMP9↓, REV has been shown to downregulate MMP-9 expression
"highlight2" >ChemoSen↑, REV enhances the anticancer effects of doxorubicin in breast cancer cells
"highlight2" >RAS↓, we reported that REV suppresses LPA-induced EGF receptor activation and subsequent inhibition a Ras/RhoA/ROCK signaling in ovarian cancer cells
"highlight2" >ROCK1↓,
"highlight2" >TumCI↓, REV may be used to reduce invasion and metastasis of breast cancer cells to improve outcomes for this devastating disease.
"highlight2" >TumMeta↓,

3098- RES,    Regulation of Cell Signaling Pathways and miRNAs by Resveratrol in Different Cancers
- Review, Var, NA
"highlight2" >NOTCH2↓, resveratrol has been reported to target multiple proteins in ovarian cancer, markedly reducing NOTCH2 and HES1 in OVCAR-3 and CAOV-3 cells
"highlight2" >Wnt↓, In CAOV-3 cells, resveratrol downregulated WNT2 and reduced the nuclear accumulation of β-catenin
"highlight2" >β-catenin/ZEB1↓,
"highlight2" >p‑SMAD2↓, Resveratrol effectively inhibits SMAD proteins
"highlight2" >p‑SMAD3↓, Resveratrol has been reported to reduce phosphorylated-SMAD2/3 in colorectal cancer LoVo cells
"highlight2" >PTCH1↓, PTCH, SMO, and GLI-1 were also inhibited in resveratrol-treated colorectal cancer HCT116 cells
"highlight2" >Smo↓,
"highlight2" >Gli1↓,
"highlight2" >E-cadherin↑, resveratrol upregulated E-cadherin
"highlight2" >NOTCH⇅, Although some reports document efficient inhibition of different proteins of the NOTCH pathway by resveratrol to inhibit cancer, there are conflicting reports that resveratrol can activate the NOTCH pathway, leading to its anticancer activity.
"highlight2" >TAC?,
"highlight2" >NKG2D↑, Resveratrol has been found to increase the cell-surface expression of NKG2D ligands and DR4 along
"highlight2" >DR4↑,
"highlight2" >survivin↓, Resveratrol dose-dependently downregulated survivin in HepG2 cells.
"highlight2" >DR5↑, resveratrol upregulated DR4, DR5, Bax, and p27(/KIP1) and inhibited the expression of cyclin D1 and Bcl-2
"highlight2" >BAX↑,
"highlight2" >p27↑,
"highlight2" >cycD1↓,
"highlight2" >Bcl-2↓,
"highlight2" >STAT3↓, Resveratrol exerts inhibitory effects on the constitutive activation of STAT3 and STAT5.
"highlight2" >STAT5↓,
"highlight2" >JAK↓, Resveratrol has also been shown to prevent the activation of JAK,
"highlight2" >DNAdam↑, Resveratrol induced DNA damage, as evidenced by the presence of multiple γ-H2AX foci after treatment with 25 μM resveratrol.
"highlight2" >γH2AX↑,

3097- RES,    Resveratrol Induces Notch2-mediated Apoptosis and Suppression of Neuroendocrine Markers in Medullary Thyroid Cancer
- in-vitro, Thyroid, TT
"highlight2" >TumCG↓, 25 μM, 50 μM, and 100 μM Resveratrol treatments for 4 days reduced growth by 5%, 8.9%, and 16.4%, resp
"highlight2" >cl‑Casp3↑, Resveratrol resulted in growth suppression and an increase in the cleavage of caspase-3 and PARP.
"highlight2" >p‑PARP↑,
"highlight2" >NOTCH2↑, Resveratrol suppresses growth, induces apoptosis, reduces ASCL1 and CgA expression, and increases Notch2 mRNA in MTC cells.

3096- RES,    Identification of potential target genes of non-small cell lung cancer in response to resveratrol treatment by bioinformatics analysis
- in-vitro, Lung, A549 - in-vitro, Lung, H1299
"highlight2" >TumCP↓, resveratrol might inhibit proliferation but induce apoptosis and autophagy via inhibiting Akt/mTOR pathway and activating p38-MAPK pathway in A549 and H1299 NSCLC cells [7]
"highlight2" >Apoptosis↑,
"highlight2" >Akt↓,
"highlight2" >mTOR↓,
"highlight2" >p38↑,
"highlight2" >MAPK↑,
"highlight2" >STAT3↓, inhibiting the messenger RNA (mRNA) and protein expression of signal transducer and activator of transcription 3 (STAT3) in A549 cells
"highlight2" >ROS↑, by leading to mitochondrial dysfunction and increasing of reactive oxygen species (ROS)
"highlight2" >SIRT1↑, suggested that resveratrol inhibited age-dependent spontaneous tumorigenesis by increasing the expression of SIRT1 and activating its downstream targets
"highlight2" >SOX2↓, resveratrol treatment promoted EGFR and inhibited SOX2.

3095- RES,    Resveratrol suppresses migration, invasion and stemness of human breast cancer cells by interfering with tumor-stromal cross-talk
- in-vitro, BC, NA
"highlight2" >TumCP↓, Resveratrol inhibited proliferation, migration and invasion of human breast cancer cells treated with CAF conditioned media.
"highlight2" >TumCMig↓,
"highlight2" >TumCI↓,
"highlight2" >cycD1↓, Resveratrol suppressed the expression of cyclin D1, c-Myc, MMP-2, MMP-9 and Sox-2 in breast cancer cells stimulated with CAFs
"highlight2" >cMyc↓,
"highlight2" >MMP2↓,
"highlight2" >MMP9↓,
"highlight2" >SOX2↓,
"highlight2" >Akt↓, Resveratrol inhibited activation of Akt and STAT3 induced in human breast cancer cells stimulated with CAF conditioned media.
"highlight2" >STAT3↓,
"highlight2" >α-SMA↓, resveratrol suppressed the proliferation of liver myofibroblasts through inhibition of α-smooth muscle actin (α-SMA)

3094- RES,    Resveratrol suppresses growth of cancer stem-like cells by inhibiting fatty acid synthase
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
"highlight2" >CSCs↓, resveratrol significantly reduced the cell viability and mammosphere formation followed by inducing apoptosis in cancer stem-like cells
"highlight2" >tumCV↓,
"highlight2" >FASN↑, This inhibitory effect of resveratrol is accompanied by a significant reduction in lipid synthesis which is caused by the down-regulation of the fatty acid synthase (FAS) gene
"highlight2" >BNIP3↑, followed by up-regulation of pro-apoptotic genes, DAPK2 and BNIP3.
"highlight2" >*cardioP↑, cardio-protective effect of resveratrol has been extensively studied in various pre-clinical models, and it has been shown that the strong anti-oxidant activity of resveratrol
"highlight2" >*antiOx↑,
"highlight2" >NF-kB↓, down-regulation of NF-kappaB, COX and matrix metalloprotease-9 (MMP9) expression
"highlight2" >COX2↓,
"highlight2" >MMP9↓,
"highlight2" >IGF-1↓, resveratrol as diet significantly reduced the onset of prostate cancer and exhibited a decrease in IGF1 (insulin-like growth factor 1) and phosphorylated-ERK1 (extracellular regulating kinase 1)
"highlight2" >ERK↓,
"highlight2" >lipid-P↓, resveratrol is indeed capable of suppressing lipid metabolism by blocking the FAS expression followed by induction of apoptosis in cancer stem-like cells
"highlight2" >CD24↓, Resveratrol induces apoptosis in tumor stem-like cells by suppressing FAS (we first isolated cancer stem-like cells (CD24-/CD44+/ESA+) from MDA-MB231)

3093- RES,    Pro-Oxidant Effect of Resveratrol on Human Breast Cancer MCF-7 Cells is Associated with CK2 Inhibition
- in-vitro, BC, MCF-7
"highlight2" >ROS↑, pro-oxidant cytotoxic effects of resveratrol in association with the inhibition of CK2 activity on human breast carcinoma cells MCF-7
"highlight2" >CK2↓,

3092- RES,    Resveratrol in breast cancer treatment: from cellular effects to molecular mechanisms of action
- Review, BC, MDA-MB-231 - Review, BC, MCF-7
"highlight2" >TumCP↓, The anticancer mechanisms of RES in regard to breast cancer include the inhibition of cell proliferation, and reduction of cell viability, invasion, and metastasis.
"highlight2" >tumCV↓,
"highlight2" >TumCI↓,
"highlight2" >TumMeta↓,
"highlight2" >*antiOx↑, antioxidative, cardioprotective, estrogenic, antiestrogenic, anti-inflammatory, and antitumor properties it has been used against several diseases, including diabetes, neurodegenerative diseases, coronary diseases, pulmonary diseases, arthritis, and
"highlight2" >*cardioP↑,
"highlight2" >*Inflam↓,
"highlight2" >*neuroP↑,
"highlight2" >*Keap1↓, RES administration resulted in a downregulation of Keap1 expression, therefore, inducing Nrf2 signaling, and leading to a decrease in oxidative damage
"highlight2" >*NRF2↑,
"highlight2" >*ROS↓,
"highlight2" >p62↓, decrease the severity of rheumatoid arthritis by inducing autophagy via p62 downregulation, decreasing the levels of interleukin-1β (IL-1β) and C-reactive protein as well as mitigating angiopoietin-1 and vascular endothelial growth factor (VEGF) path
"highlight2" >IL1β↓,
"highlight2" >CRP↓,
"highlight2" >VEGF↓,
"highlight2" >Bcl-2↓, RES downregulates the levels of Bcl-2, MMP-2, and MMP-9, and induces the phosphorylation of extracellular-signal-regulated kinase (ERK)/p-38 and FOXO4
"highlight2" >MMP2↓,
"highlight2" >MMP9↓,
"highlight2" >FOXO4↓,
"highlight2" >POLD1↓, The in vivo experiment involving a xenograft model confirmed the ability of RES to reduce tumor growth via POLD1 downregulation
"highlight2" >CK2↓, RES reduces the expression of casein kinase 2 (CK2) and diminishes the viability of MCF-7 cells.
"highlight2" >MMP↓, Furthermore, RES impairs mitochondrial membrane potential, enhances ROS generation, and induces apoptosis, impairing BC progression
"highlight2" >ROS↑,
"highlight2" >Apoptosis↑,
"highlight2" >TumCCA↑, RES has the capability of triggering cell cycle arrest at S phase and reducing the number of 4T1 BC cells in G0/G1 phase
"highlight2" >Beclin-1↓, RES administration promotes cytotoxicity of DOX against BC cells by downregulating Beclin-1 and subsequently inhibiting autophagy
"highlight2" >Ki-67↓, Reducing the Ki-67
"highlight2" >ATP↓, RES’s administration is responsible for decreasing ATP production and glucose metabolism in MCF-7 cells.
"highlight2" >GlutMet↓,
"highlight2" >PFK↓, RES decreased PFK activity, preventing glycolysis and glucose metabolism in BC cells and decreasing cellular growth rate
"highlight2" >TGF-β↓, RES (12.5–100 µM) inhibited TGF-β signaling and reduced the expression levels of its downstream targets that include Smad2 and Smad3 and as a result impaired the progression of BC cells.
"highlight2" >SMAD2↓,
"highlight2" >SMAD3↓,
"highlight2" >Vim?, a significant decrease in the levels of vimentin, Snail1 and Slug occurred, while E-cadherin levels increased to suppress EMT and metastasis of BC cells.
"highlight2" >Snail↓,
"highlight2" >Slug↓,
"highlight2" >E-cadherin↑,
"highlight2" >EMT↓,
"highlight2" >Zeb1↓, a significant decrease in the levels of vimentin, Snail1 and Slug occurred, while E-cadherin levels increased to suppress EMT and metastasis of BC cells.
"highlight2" >Fibronectin↓,
"highlight2" >IGF-1↓, RES administration (10 and 20 µM) impaired the migration and invasion of BC cells via inhibiting PI3K/Akt and therefore decreasing IGF-1 expression and preventing the upregulation of MMP-2
"highlight2" >PI3K↓,
"highlight2" >Akt↓,
"highlight2" >HO-1↑, The activation of heme oxygenase-1 (HO-1) signaling by RES reduced MMP-9 expression and prevented metastasis of BC cells
"highlight2" >eff↑, RES-loaded gold nanoparticles were found to enhance RES’s ability to reduce MMP-9 expression as compared to RES alone
"highlight2" >PD-1↓, RES inhibited PD-1 expression to promote CD8+ T cell activity and enhance Th1 immune responses.
"highlight2" >CD8+↑,
"highlight2" >Th1 response↑,
"highlight2" >CSCs↓, RES has the ability to target CSCs in various tumors
"highlight2" >RadioS↑, RES in reversing drug resistance and radio resistance.
"highlight2" >SIRT1↑, RES administration (12.5–200 µmol/L) promotes sensitivity of BC cells to DOX by increasing Sirtuin 1 (SIRT1) expression
"highlight2" >Hif1a↓, downregulating HIF-1α expression, an important factor in enhancing radiosensitivity
"highlight2" >mTOR↓, mTOR suppression

3091- RES,    Protein kinase CK2 modulates apoptosis induced by resveratrol and epigallocatechin-3-gallate in prostate cancer cells
- in-vitro, Pca, PC3 - in-vitro, Pca, ALVA-41
"highlight2" >CK2↓, Resveratrol- and EGCG-induced apoptosis is associated with a significant down-regulation of CK2 activity and protein expression in both the ALVA-41 and PC-3 cells
"highlight2" >Apoptosis↑,

3090- RES,    The Effects of Resveratrol Targeting MicroRNA-4325P/PDGF-B to Regulate Tumor Angiogenesis in Osteosarcoma Microenvironment
- in-vitro, OS, MG63
"highlight2" >PDGFR-BB↓, There is evidence that resveratrol prevents tumor growth by phosphorylation of the PDGFR gene and suppresses the angiogenesis triggered by PDGFB, thereby inhibiting the growth of tumors.
"highlight2" >angioG↓,

3089- RES,    The Role of Resveratrol in Cancer Therapy
- Review, Var, NA
"highlight2" >angioG↓, resveratrol plays a role in inhibiting the expression of MMP (mainly MMP-9) [174,175,176,177] and angiogenesis markers such as VEGF, EGFR or FGF-2
"highlight2" >VEGF↓,
"highlight2" >EGFR↓,
"highlight2" >FGF↑,
"highlight2" >TumCMig↓, Resveratrol reduced the phorbo-12-myristate 13-acetate (PMA)-induced migration and invasion ability of liver cancer HepG2 and Hep3B cells.
"highlight2" >TumCI↓,
"highlight2" >TIMP1↑, resveratrol up-regulated TIMP-1 protein expression and down-regulated MMP-9 activity, while the activities of MMP-2 and MMP-9 were decreased,
"highlight2" >MMP2↓,
"highlight2" >MMP9↓,
"highlight2" >NF-kB↓, via down-regulating the expression of NF-κB,
"highlight2" >Hif1a↓, It has been reported that resveratrol suppresses the expression of VEGF and HIF-1α in human ovarian cancer cells via abrogating the activation of the PI3K/Akt and MAPK signaling pathways
"highlight2" >PI3K↓,
"highlight2" >Akt↓,
"highlight2" >MAPK↓,
"highlight2" >EMT↓, Many studies have shown that resveratrol suppresses the development of tumor invasion and metastasis through inhibiting signaling pathways associated with EMT
"highlight2" >AR↓, Resveratrol suppressed prostate cancer growth via down-regulating the androgen receptor (AR) expression in the TRAMP model of prostate cancer

2988- RES,    The Antimetastatic Effects of Resveratrol on Hepatocellular Carcinoma through the Downregulation of a Metastasis-Associated Protease by SP-1 Modulation
- in-vitro, HCC, HUH7
"highlight2" >TumCMig↓, resveratrol treatment significantly inhibited cell migration and invasion capacities of Huh7 cell lines that have low cytotoxicity in vitro, even at a high concentration of 100 µM.
"highlight2" >TumCI↓,
"highlight2" >uPA↓, activities and protein levels of the urokinase-type plasminogen activator (u-PA) were inhibited by resveratrol.
"highlight2" >Sp1/3/4↓, reactive in transcription protein of nuclear factor SP-1 was inhibited by resveratrol.

3087- RES,    Resveratrol cytotoxicity is energy-dependent
- Review, Var, NA
"highlight2" >OXPHOS↓, The inhibition of the oxidative phosphorylation (OXPHOS) pathway appears to be the molecular mechanism of resveratrol.
"highlight2" >eff↝, This review suggests that investigating a possible complex relationship between caloric intake and the differential effects of resveratrol on OXPHOS may be justified.
"highlight2" >eff↑, A low-calorie diet accompanied by significant levels of resveratrol might modify cellular bioenergetics, which could impact cellular viability and enhance the anti-cancer properties of resveratrol.

3086- RES,    Resveratrol inhibits the tumor migration and invasion by upregulating TET1 and reducing TIMP2/3 methylation in prostate carcinoma cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, PC3 - in-vitro, Pca, DU145
"highlight2" >TET1↑, Res upregulated the 5hmC and TET1 levels and downregulated the 5mC level.
"highlight2" >TumCMig↓, Res also inhibited the migration and invasion of PCa cells
"highlight2" >TumCI↓,
"highlight2" >TIMP2↑, promoted the demethylation of TIMP2 and TIMP3 to upregulate their expressions, and suppressed the expressions of MMP2 and MMP9.
"highlight2" >TIMP3↑,
"highlight2" >MMP2↓,
"highlight2" >MMP9↓,

3085- RES,    Resveratrol interrupts Wnt/β-catenin signalling in cervical cancer by activating ten-eleven translocation 5-methylcytosine dioxygenase 1
- in-vitro, Cerv, NA
"highlight2" >TET1↑, After treating cervical cancer cells with Resveratrol (RES), we found that TET1 expression was elevated and Wnt/β-catenin pathway activity was suppressed.
"highlight2" >Wnt↓,
"highlight2" >β-catenin/ZEB1↓,

3084- RES,    Resveratrol inhibits the proliferation of estrogen receptor-positive breast cancer cells by suppressing EZH2 through the modulation of ERK1/2 signaling
- in-vitro, BC, MCF-7 - in-vitro, BC, T47D
"highlight2" >TumCP↓, Resveratrol inhibited the proliferation and colony formation in ER-positive breast cancer cells and downregulated EZH2 through inhibition of phospho-ERK1/2.
"highlight2" >EZH2↓,
"highlight2" >p‑ERK↓,

885- RES,    Resveratrol induces intracellular Ca2 + rise via T-type Ca2 + channels in a mesothelioma cell line
- in-vitro, RCC, REN - in-vitro, Nor, MeT5A
"highlight2" >TumCG↓, for RCC only
"highlight2" >Ca+2↑, Res induces Ca2+ influx, possibly mediated through T-type Ca2+ channels, with significant selectivity towards mesothelioma cells
"highlight2" >*toxicity↓, MeT-5 A mesothelial cells (EC50 = 4.9 μM) with respect to REN cells (EC50 = 2.7 μM).

2330- RES,    Resveratrol Induces Cancer Cell Apoptosis through MiR-326/PKM2-Mediated ER Stress and Mitochondrial Fission
- in-vitro, CRC, DLD1 - in-vitro, Cerv, HeLa - in-vitro, BC, MCF-7
"highlight2" >TumCP↓, Res inhibited cell proliferation and induced cell apoptosis
"highlight2" >Apoptosis↑,
"highlight2" >PKM2↓, reduction of PKM2 expression in tumor cells by Res treatment
"highlight2" >ER Stress↑, increased the expression of ER stress and mitochondrial fission proteins but reduced cell viability and the levels of fusion proteins.

3052- RES,    Resveratrol-Induced Downregulation of NAF-1 Enhances the Sensitivity of Pancreatic Cancer Cells to Gemcitabine via the ROS/Nrf2 Signaling Pathways
- in-vitro, PC, PANC1 - in-vitro, PC, MIA PaCa-2 - in-vitro, PC, Bxpc-3
"highlight2" >NAF1↓, resveratrol suppresses the expression of NAF-1 in pancreatic cancer cells by inducing cellular reactive oxygen species (ROS) accumulation and activating Nrf2 signaling.
"highlight2" >ROS↑,
"highlight2" >NRF2↑,
"highlight2" >eff↑, may enhance the efficacy of gemcitabine in pancreatic cancer therapy.
"highlight2" >TumCG↓, Resveratrol decreased the growth of the cancer cells in a dose- and time-dependent manner.

2328- RES,    Resveratrol Inhibits Cancer Cell Metabolism by Down Regulating Pyruvate Kinase M2 via Inhibition of Mammalian Target of Rapamycin
- in-vitro, Cerv, HeLa - in-vitro, Liver, HepG2 - in-vitro, BC, MCF-7
"highlight2" >PKM2↓, resveratrol down-regulated PKM2 expression by inhibiting mTOR signaling and suppressed cancer metabolism
"highlight2" >mTOR↓,
"highlight2" >GlucoseCon↓, decreased glucose uptake, lactate production (aerobic glycolysis) and reduced anabolism (macromolecule synthesis) in various cancer cell lines
"highlight2" >lactateProd↓,

1511- RES,  Chemo,    Combination therapy in combating cancer
- Review, NA, NA
"highlight2" >eff↑, Our studies, as well as others, have shown the effectiveness of resveratrol in combination therapy in vitro and in vivo
"highlight2" >*NRF2↑, chemopreventive effects through the activation of Nrf2 and consequently GSH expression
"highlight2" >*GSH↑,
"highlight2" >*ROS↓, In addition, curcuminoids upregulate glutathione levels which have been shown to reduce ROS levels and remove carcinogens, aiding in chemoprevention
"highlight2" >chemoP↑,
"highlight2" >ChemoSideEff↓, Our lab showed that this antioxidant compound has cytoprotective properties against the side effects of chemotherapy

1506- RES,    Epigenetic targets of bioactive dietary components for cancer prevention and therapy
- Review, NA, NA
"highlight2" >DNMTs↓, weaker DNMT inhibitory activity than other dietary bioactive components such as EGCG
"highlight2" >BRCA1↑, resveratrol treatment, which was associated with BRAC-1 reactivation in MCF-7 cells
"highlight2" >HDAC↓, resveratrol is associated with activation of the type III HDAC inhibitors, sirtuin 1 (SIRT1), and p300, in multiple in vitro and in vivo models
"highlight2" >SIRT1↑,
"highlight2" >p300↓, Significant decreases in the amounts of p300, HDAC1, HDAC3, and HDAC8
"highlight2" >survivin↓,
"highlight2" >HDAC1↓,
"highlight2" >HDAC3↓,
"highlight2" >HDAC8↓,

1492- RES,    Resveratrol: Biological and pharmaceutical properties as anticancer molecule
- Review, Var, NA
"highlight2" >RadioS↑,
"highlight2" >ChemoSen↑,

1491- RES,    Resveratrol Augments Doxorubicin and Cisplatin Chemotherapy: A Novel Therapeutic Strategy
"highlight2" >RadioS↑,
"highlight2" >ChemoSen↑,

1490- RES,    Anticancer Potential of Resveratrol, β-Lapachone and Their Analogues
- Review, Var, NA
"highlight2" >TumCCA↑, lapachone and its iodine derivatives induce cell cycle arrest in G2/M in human oral squamous cell carcinoma cells
"highlight2" >ROS↑, The primary mechanism of action of β-lapachone and its derivatives is the formation of ROS [92] through its processing by NAD(P)H quinone oxidoreductase 1 (NQO1).
"highlight2" >Ca+2↑, abnormal production of ROS leads to an increase in Ca++
"highlight2" >MMP↓, depolarization of the mitochondrial membrane
"highlight2" >ATP↓, decrease in ATP synthesis
"highlight2" >TOP1?, β-lapachone inhibits the catalytic activity of topoisomerase I
"highlight2" >P53↑, including upregulation of the p53 tumor suppressor protein
"highlight2" >p53 Wildtype∅,
"highlight2" >Akt↓, inactivation of the Akt/mTOR pathway was again attributed to β-lapachone, promoting the inhibition of EMT transition in NQO1-positive cells.
"highlight2" >mTOR↓,
"highlight2" >EMT↓,
"highlight2" >*BioAv↓, β-lapachone is a promising anticancer drug, its low bioavailability represents a limitation for clinical use due to low solubility in water and gastrointestinal fluids

1489- RES,    Molecular mechanisms of resveratrol as chemo and radiosensitizer in cancer
- Review, Var, NA
"highlight2" >RadioS↑,
"highlight2" >ChemoSen↑,
"highlight2" >*BioAv↓, However, in vivo experimental models have demonstrated that RSV is rapidly metabolized and eliminated, which leads to low bioavailability of the compound. 75% of RSV has been shown to be absorbed orally, only 1% is detected in the blood plasma
"highlight2" >*BioAv↑, nanocarrier of RSV-loaded poly (ε-caprolactone)-poly (ethylene glycol) nanoparticles with an erythrocyte membrane. This system improved RSV’s poor water solubility
"highlight2" >Ferroptosis↑, SV could induce ferroptotic cell death in colorectal cancer by initiating lipid peroxidation and suppressing the expression of SLC7A11 and GPX4
"highlight2" >lipid-P↑,
"highlight2" >xCT↓,
"highlight2" >GPx4↓,
"highlight2" >*BioAv↑, Bioactive or bioenhancer compounds have also been used (piperine, quercetin, biflavone ginkgetin) that, in combination with RSV, improve bioavailability, solubility, absorption, and cellular permeability
"highlight2" >COX2↓, inhibiting Cyclooxygenase-COX
"highlight2" >cycD1↓,
"highlight2" >FasL↓,
"highlight2" >FOXP3↓,
"highlight2" >HLA↑,
"highlight2" >p‑NF-kB↓, decrease NF-ĸB phosphorylation
"highlight2" >BAX↑,
"highlight2" >Bcl-2↓,
"highlight2" >MALAT1↓, decrease the expression of the lncRNA MALAT1 in colorectal and gastric cancer cells through the Wnt/β-catenin signaling pathway

1391- RES,  BBR,    Effects of Resveratrol, Berberine and Their Combinations on Reactive Oxygen Species, Survival and Apoptosis in Human Squamous Carcinoma (SCC-25) Cells
- in-vitro, Tong, SCC25
"highlight2" >ROS↑,
"highlight2" >eff↑, cytotoxicity of the compounds was significantly improved after their combined application Additive effects were observed for doses lower than the calculated IC50 of berberine [IC50=23µg/ml] and resveratrol [IC50=9µg/ml].

1282- RES,    Resveratrol Inhibits CD4+ T Cell Activation by Enhancing the Expression and Activity of Sirt1
- vitro+vivo, NA, NA
"highlight2" >T-Cell↓, inhibits the activation and cytokine production of T cells
"highlight2" >SIRT1↑,
"highlight2" >CD4+↓,

1047- RES,    Resveratrol induces PD-L1 expression through snail-driven activation of Wnt pathway in lung cancer cells
- in-vitro, Lung, H1299 - in-vitro, Lung, A549 - in-vitro, Lung, H460
"highlight2" >PD-L1↑, resveratrol dose-dependently upregulates PD-L1 expression at the range of pharmacologic-achievable concentrations in lung cancer cells
"highlight2" >Snail↑, resveratrol dose-dependently increased Snail levels in association with the suppression of E-cadherin protein levels, as well as induction of N-cadherin, Fibronectin and Vimentin levels
"highlight2" >E-cadherin↓,
"highlight2" >N-cadherin↑, induction of N-cadherin, Fibronectin and Vimentin levels
"highlight2" >Fibronectin↑,
"highlight2" >Vim↑,
"highlight2" >Axin2↓, Snail in turn inhibits transcription of Axin2

993- RES,    Resveratrol reverses the Warburg effect by targeting the pyruvate dehydrogenase complex in colon cancer cells
- in-vitro, CRC, Caco-2 - in-vivo, Nor, HCEC 1CT
"highlight2" >TumCG↓,
"highlight2" >Glycolysis↓,
"highlight2" >PPP↓,
"highlight2" >ATP↑, significant increase (20%) in ATP production
"highlight2" >PDH↑, Resveratrol targets the pyruvate dehydrogenase (PDH) complex, a key mitochondrial gatekeeper of energy metabolism, leading to an enhanced PDH activity.
"highlight2" >Ca+2↝, resveratrol is a potent modulator of many cellular Ca2+ signaling pathways. Ca2+ is a key mediator of the effect of resveratrol on the oxidative capacity of colon cancer cells.
"highlight2" >TumCP↓,
"highlight2" >lactateProd↓,
"highlight2" >OCR↑, increase of oxygen consumption rate (OCR) both in normal colonic epithelial HCEC 1CT cells
"highlight2" >ECAR↓, Following treatment with resveratrol (10 µM, 48 hr), the ECAR was unchanged in normal HCEC 1CT cells, whereas it was significantly reduced (31%) in HCEC 1CT RPA cells ****
"highlight2" >*ECAR∅, Following treatment with resveratrol (10 µM, 48 hr), the ECAR was unchanged in normal HCEC 1CT cells
"highlight2" >*other?, Resveratrol promotes a shift from respiration to glycolysis in cancer-like cells, but not in normal colonocytes
"highlight2" >cycE↑, Resveratrol inhibited cell cycle progression by enhancing the levels of cyclin E and cyclin A
"highlight2" >cycA1↑,
"highlight2" >TumCCA↑,
"highlight2" >cycD1↑, and by decreasing cyclin D1
"highlight2" >OXPHOS↑, Taken together, these observations indicate that exposure to resveratrol leads to a metabolic reorientation from aerobic glycolysis toward OXPHOS.

967- RES,    Resveratrol binds and inhibits transcription factor HIF-1α in pancreatic cancer
- Analysis, PC, NA
"highlight2" >Hif1a↓,

924- RES,    Resveratrol sequentially induces replication and oxidative stresses to drive p53-CXCR2 mediated cellular senescence in cancer cells
- in-vitro, OS, U2OS - in-vitro, Lung, A549
"highlight2" >TumCCA↑, S-phase arrest, which is commonly observed in cells treated with RSV
"highlight2" >ROS↑,
"highlight2" >γH2AX↑, remarkable increase in the amount of γ-H2AX, a marker for DNA double-strand breaks
"highlight2" >ATM↑, a master regulator of DNA damage response, was activated by RSV
"highlight2" >p‑CHK1↑,
"highlight2" >cellSen↑,
"highlight2" >CXCR2↑, peaks at day 5 then drops

2329- RES,    Resveratrol induces apoptosis in human melanoma cell through negatively regulating Erk/PKM2/Bcl-2 axis
- in-vitro, Melanoma, A375
"highlight2" >P53↑, In the present study, we found that resveratrol dramatically inhibited melanoma cell proliferation and induced cell apoptosis through upregulation of p53 in a concentration-dependent manner.
"highlight2" >Bcl-2↓, resveratrol downregulated antiapoptotic protein Bcl-2 and activated Bax in the protein levels by promoting Bcl-2 degradation and cytochrome c release.
"highlight2" >BAX↑,
"highlight2" >Cyt‑c↑,
"highlight2" >ERK↓, apoptosis induction of resveratrol in melanoma cells and suggested that downregulating Erk/PKM2/Bcl-2 axis appears to be a new approach for the prevention or treatment of melanoma.
"highlight2" >PKM2↓,
"highlight2" >Apoptosis↑,
"highlight2" >γH2AX↑, levels of γH2AX increased significantly in melanoma cells after the addition of resveratrol
"highlight2" >Casp3↑, Active Caspase3 and cleaved PARP1 were increased in resveratrol-treated cells
"highlight2" >cl‑PARP1↑,

884- RES,  PTS,    Resveratrol and Pterostilbene Exhibit Anticancer Properties Involving the Downregulation of HPV Oncoprotein E6 in Cervical Cancer Cells
- in-vitro, Cerv, HeLa
"highlight2" >TumCD↑, pterostilbene displayed a 1.97-fold lower IC50 than Res
"highlight2" >TumCCA↑, S-phase cell cycle arrest (both)
"highlight2" >E6↓, Downregulation of HPV Oncoprotein E6
"highlight2" >Casp3↑,
"highlight2" >P53↑,

883- RES,    Targeting Histone Deacetylases with Natural and Synthetic Agents: An Emerging Anticancer Strategy
"highlight2" >HDAC↓, Res is a naturally occurring HDACi
"highlight2" >TumCCA↑, HDACi exhibit their antitumor effect by the activation of cell cycle arrest, induction of apoptosis and autophagy, angiogenesis inhibition, increased reactive oxygen species generation causing oxidative stress, and mitotic cell death in cancer cells.
"highlight2" >Apoptosis↑,
"highlight2" >angioG↓,
"highlight2" >ROS↑,

882- RES,    Resveratrol: A Double-Edged Sword in Health Benefits
- Review, NA, NA
"highlight2" >AntiTum↑,
"highlight2" >Casp3↑,
"highlight2" >Casp9↑,
"highlight2" >BAX↑,
"highlight2" >Bcl-2↓,
"highlight2" >Bcl-xL↓,
"highlight2" >P53↑,
"highlight2" >NAF1↓,
"highlight2" >NRF2↑,
"highlight2" >ROS↑,
"highlight2" >Apoptosis↑,
"highlight2" >HDAC↓, Resveratrol is also an Histone deacetylase inhibitors
"highlight2" >TumCCA↑,
"highlight2" >TumAuto↑,
"highlight2" >angioG↓,
"highlight2" >iNOS↓, inhibit iNOS expression in colon cancer cells

881- RES,    Resveratrol inhibits Src and Stat3 signaling and induces the apoptosis of malignant cells containing activated Stat3 protein
- in-vitro, BC, MDA-MB-231 - in-vitro, PC, PANC1 - in-vitro, Pca, DU145
"highlight2" >TumCCA↑, at the G0 -G1 phase or at the S phase (malignant cells contain activated Stat3)
"highlight2" >cycD1↓,
"highlight2" >Bcl-xL↓,
"highlight2" >Mcl-1↓,
"highlight2" >other↓, not effective on cells lacking aberrant Stat3 activity

880- RES,    Forkhead Proteins Are Critical for Bone Morphogenetic Protein-2 Regulation and Anti-tumor Activity of Resveratrol
- in-vitro, BC, MDA-MB-231
"highlight2" >other↓, reduced tumor formation
"highlight2" >TumW↓, 55%
"highlight2" >FOXO↑, resveratrol resulted in strong induction of FOXO3a activity
"highlight2" >BMP2↑, BMP-2 gene was identified as one of the highly increased genes in resveratrol-treated

879- RES,    Evidence that TNF-β induces proliferation in colorectal cancer cells and resveratrol can down-modulate it
- in-vitro, CRC, HCT116
"highlight2" >TumCP↓, resveratrol reversed the TNF-β-induced proliferation
"highlight2" >NF-kB↓,

878- RES,    Resveratrol suppresses epithelial-to-mesenchymal transition in colorectal cancer through TGF-β1/Smads signaling pathway mediated Snail/E-cadherin expression
- vitro+vivo, CRC, LoVo
"highlight2" >TumMeta↓,
"highlight2" >E-cadherin↑,
"highlight2" >Vim↓,
"highlight2" >TGF-β↓,
"highlight2" >SMAD2↓,
"highlight2" >EMT↓,
"highlight2" >SMAD3↓,

877- RES,    Resveratrol Inhibits Invasion and Metastasis of Colorectal Cancer Cells via MALAT1 Mediated Wnt/β-Catenin Signal Pathway
- in-vitro, CRC, LoVo - in-vitro, CRC, HCT116
"highlight2" >MALAT1↓,
"highlight2" >Wnt/(β-catenin)↓,
"highlight2" >TumCI↓,
"highlight2" >TumMeta↓,

871- RES,  CUR,  QC,    The effect of resveratrol, curcumin and quercetin combination on immuno-suppression of tumor microenvironment for breast tumor-bearing mice
- in-vitro, BC, 4T1 - in-vivo, BC, 4T1
"highlight2" >T-Cell↑, in tumor microenviroment
"highlight2" >Neut↓,
"highlight2" >Macrophages↓,
"highlight2" >ROS↑, RCQ significantly increased reactive oxygen species
"highlight2" >MMP↓, in cancer cells
"highlight2" >other↓, alleviate immunosuppression of the tumor microenvironment to enhance the anti-tumor effect.
"highlight2" >AntiTum↑, at least nearly 5 times higher than that of a single Res/Cur/Que  = 1:1:0.5
"highlight2" >TumVol↓, 35-47% tumor inhibition rate

105- RES,  QC,    The Effect of Resveratrol and Quercetin on Epithelial-Mesenchymal Transition in Pancreatic Cancer Stem Cell
- in-vitro, Pca, CD133+
"highlight2" >N-cadherin↓,
"highlight2" >TNF-α↓,
"highlight2" >ACTA2↓,

104- RES,  QC,    Resveratrol and Quercetin in Combination Have Anticancer Activity in Colon Cancer Cells and Repress Oncogenic microRNA-27a
- in-vitro, Colon, HT-29
"highlight2" >Casp3↑, x2
"highlight2" >PARP↑,
"highlight2" >survivin↓,
"highlight2" >miR-27a-3p↓, miR-27a
"highlight2" >Sp1/3/4↓,
"highlight2" >ZBTB10↑,

103- RES,  CUR,  QC,    The effect of resveratrol, curcumin and quercetin combination on immuno-suppression of tumor microenvironment for breast tumor-bearing mice
- vitro+vivo, BC, 4T1
"highlight2" >ROS↑,
"highlight2" >MMP↓,
"highlight2" >Bcl-2↓,
"highlight2" >BAX↑,
"highlight2" >Casp9↑,
"highlight2" >T-Cell↑, (CD4+CD8+)
"highlight2" >TGF-β↓,

102- RES,    Effect of resveratrol on proliferation and apoptosis of human pancreatic cancer MIA PaCa-2 cells may involve inhibition of the Hedgehog signaling pathway
- in-vitro, PC, MIA PaCa-2
"highlight2" >HH↓,
"highlight2" >PTCH1↓,
"highlight2" >Smo↓,
"highlight2" >HH↓, Ihh
"highlight2" >EMT↓,
"highlight2" >PI3K/Akt↓, thru PI-3K/Akt/NF-κB↓
"highlight2" >NF-kB↓,

101- RES,    Resveratrol inhibits the hedgehog signaling pathway and epithelial-mesenchymal transition and suppresses gastric cancer invasion and metastasis
- in-vitro, GC, SGC-7901
"highlight2" >HH↓,
"highlight2" >Gli1↓,
"highlight2" >EMT↓,
"highlight2" >Snail↓,
"highlight2" >N-cadherin↓,
"highlight2" >E-cadherin↑,

2332- RES,    Resveratrol’s Anti-Cancer Effects through the Modulation of Tumor Glucose Metabolism
- Review, Var, NA
"highlight2" >Glycolysis↓, Resveratrol reduces glucose uptake and glycolysis by affecting Glut1, PFK1, HIF-1α, ROS, PDH, and the CamKKB/AMPK pathway.
"highlight2" >GLUT1↓, resveratrol reduces glycolytic flux and Glut1 expression by targeting ROS-mediated HIF-1α activation in Lewis lung carcinoma tumor-bearing mice
"highlight2" >PFK1↓,
"highlight2" >Hif1a↓, Resveratrol specifically suppresses the nuclear β-catenin protein by inhibiting HIF-1α
"highlight2" >ROS↑, Resveratrol increases ROS production
"highlight2" >PDH↑, leading to increased PDH activity, inhibiting HK and PFK, and downregulating PKM2 activity
"highlight2" >AMPK↑, esveratrol elevated NAD+/NADH, subsequently activated Sirt1, and in turn activated the AMP-activated kinase (AMPK),
"highlight2" >TumCG↓, inhibits cell growth, invasion, and proliferation by targeting NF-kB, Sirt1, Sirt3, LDH, PI-3K, mTOR, PKM2, R5P, G6PD, TKT, talin, and PGAM.
"highlight2" >TumCI↓,
"highlight2" >TumCP↓,
"highlight2" >p‑NF-kB↓, suppressing NF-κB phosphorylation
"highlight2" >SIRT1↑, Resveratrol activates the target subcellular histone deacetylase Sirt1 in various human tissues, including tumors
"highlight2" >SIRT3↑,
"highlight2" >LDH↓, decreases glycolytic enzymes (pyruvate kinase and LDH) in Caco2 and HCT-116 cells
"highlight2" >PI3K↓, Resveratrol also targets “classical” tumor-promoting pathways, such as PI3K/Akt, STAT3/5, and MAPK, which support glycolysis
"highlight2" >mTOR↓, AMPK activation further inhibits the mTOR pathway
"highlight2" >PKM2↓, inhibiting HK and PFK, and downregulating PKM2 activity
"highlight2" >R5P↝,
"highlight2" >G6PD↓, G6PDH knockdown significantly reduced cell proliferation
"highlight2" >TKT↝,
"highlight2" >talin↓, induces apoptosis by targeting the pentose phosphate and talin-FAK signaling pathways
"highlight2" >HK2↓, Resveratrol downregulates glucose metabolism, mainly by inhibiting HK2;
"highlight2" >GRP78/BiP↑, resveratrol stimulates GRP-78, and decreases glucose uptake,
"highlight2" >GlucoseCon↓,
"highlight2" >ER Stress↑, resveratrol-induced ER-stress leads to apoptosis of CRC cells
"highlight2" >Warburg↓, Resveratrol reverses the Warburg effect
"highlight2" >PFK↓, leading to increased PDH activity, inhibiting HK and PFK, and downregulating PKM2 activity

2991- RES,  Chemo,    Synergistic anti-cancer effects of resveratrol and chemotherapeutic agent clofarabine against human malignant mesothelioma MSTO-211H cells
- in-vitro, Melanoma, MSTO-211H - in-vitro, Nor, MeT5A
"highlight2" >eff↑, resveratrol and clofarabine produced a synergistic antiproliferative effect in MSTO-211H cells, but not in MeT-5A cells.
"highlight2" >selectivity↑,
"highlight2" >Sp1/3/4↓, ability of resveratrol to reduce the contents of Sp1

2990- RES,    Resveratrol reduces cerebral edema through inhibition of de novo SUR1 expression induced after focal ischemia
- in-vivo, Stroke, NA
"highlight2" >*OS↑, We found that RSV reduced the infarct area and cerebral edema, prevented blood-brain barrier damage, improved neurological performance, and increased survival.
"highlight2" >*antiOx↑, antioxidant activity of RSV targeted SP transcription factors and inhibited SUR1 and AQP4 expression.
"highlight2" >Sp1/3/4↓,

2989- RES,    Resveratrol Represses Pokemon Expression in Human Glioma Cells
- in-vitro, GBM, NA
"highlight2" >FBI-1↓, we showed that RSV could efficiently decrease the activity of the Pokemon promoter and the expression of Pokemon.
"highlight2" >Sp1/3/4↓, RSV also inhibited Sp1 DNA binding activity to the Pokemon promoter; whereas, it did not influence the expression and nuclear translocation of Sp1.

2987- RES,    Resveratrol ameliorates myocardial damage by inducing vascular endothelial growth factor-angiogenesis and tyrosine kinase receptor Flk-1
- in-vivo, Nor, NA
"highlight2" >*VEGF↑, effect of resveratrol on significant upregulation of the protein expression profiles of vascular endothelial growth factor (VEGF) and its tyrosine kinase receptor Flk-1, 3 wk after MI.
"highlight2" >*iNOS↑, Pretreatment with resveratrol also increased nitric-oxide synthase (inducible NOS and endothelial NOS) along with increased antiapoptotic and proangiogenic factors nuclear factor (NF)-kappaB and specificity protein (SP)-1.
"highlight2" >*NF-kB↑,
"highlight2" >*Sp1/3/4↑,
"highlight2" >*cardioP↑, demonstrate increased capillary density as well as improved left ventricular function by pharmacological preconditioning with resveratrol 3 wk after MI

2986- RES,    Effect of the natural compound trans‑resveratrol on human MCM4 gene transcription
- in-vitro, Cerv, HeLa - in-vitro, AML, HL-60
"highlight2" >Sp1/3/4↑, As revealed in Fig. 5A, an increase of Sp1 and a decrease of PU.1 were observed. The Sp1/PU.1 ratio was markedly induced 24 h after the addition of Rsv to the culture medium

2985- RES,    Resveratrol Inhibits Diabetic-Induced Müller Cells Apoptosis through MicroRNA-29b/Specificity Protein 1 Pathway
- in-vivo, Nor, NA - vitro+vivo, Diabetic, NA
"highlight2" >*Sp1/3/4↓, diabetes-induced downregulated expression of miR-29b and upregulated expression of SP1 could be rescued by RSV in vivo and in vitro
"highlight2" >*miR-29b↑,

2984- RES,    Involvement of miR-539-5p in the inhibition of de novo lipogenesis induced by resveratrol in white adipose tissue
- in-vivo, Nor, NA
"highlight2" >*Sp1/3/4↓, Among the three targets, only SP1 showed a reduction in protein expression.
"highlight2" >*SREBP1↓, In addition, significant reductions in SREBP1 protein expression and fasn gene expression were found in resveratrol-treated rats.
"highlight2" >*FASN↓,

2983- RES,    Resveratrol Improves Diabetic Retinopathy via Regulating MicroRNA-29b/Specificity Protein 1/Apoptosis Pathway by Enhancing Autophagy
- in-vitro, Nor, NA
"highlight2" >*Beclin-1↑, RSV increased autophagosome formation and LC3-I/LC3-II and Beclin-1 levels while decreasing P62 level, thereby promoting autophagy and inhibiting dysregulation of miR-29b/SP1 pathway expression and RMCs apoptosis in DR rat retinal tissues and high gl
"highlight2" >*p62↓,
"highlight2" >*Sp1/3/4↓, RSV further inhibits the apoptosis of RMCs by activating autophagy and regulating the early miR-29b downregulation and SP1 upregulation induced by high glucose
"highlight2" >*Apoptosis↓,

2982- RES,    The flavonoid resveratrol suppresses growth of human malignant pleural mesothelioma cells through direct inhibition of specificity protein 1
- in-vitro, Melanoma, MSTO-211H
"highlight2" >tumCV↓, Cell viability was decreased and apoptotic cell death was increased by Res (0-60 µM).
"highlight2" >Apoptosis↑,
"highlight2" >Sp1/3/4↓, significantly suppressed Sp1 protein levels, but not Sp1 mRNA levels
"highlight2" >p27↓, figure 4
"highlight2" >P21↓,
"highlight2" >cycD1↓,
"highlight2" >Mcl-1↓,
"highlight2" >survivin↓,

2981- RES,    Resveratrol suppresses IGF-1 induced human colon cancer cell proliferation and elevates apoptosis via suppression of IGF-1R/Wnt and activation of p53 signaling pathways
- in-vitro, Colon, HT-29 - in-vitro, Colon, SW48
"highlight2" >TumCCA↑, by arresting G0/G1-S phase cell cycle progression through p27 stimulation and cyclin D1 suppression.
"highlight2" >p27↑,
"highlight2" >cycD1↓,
"highlight2" >TumCP↓, resveratrol suppressed IGF-1R protein levels and concurrently attenuated the downstream Akt/Wnt signaling pathways that play a critical role in cell proliferation.
"highlight2" >IGF-1R↓,
"highlight2" >Akt↓,
"highlight2" >Wnt↓,
"highlight2" >P53↑, Resveratrol treatment induced apoptosis by activating tumor suppressor p53 protein,
"highlight2" >Apoptosis↑,
"highlight2" >Sp1/3/4↓, Resveratrol also activated p53 protein and suppressed levels of sp1, a protein that transcriptionally activates IGF-1R
"highlight2" >cl‑PARP↑, Resveratrol treatment elevated cleaved PARP, a hallmark of apoptosis
"highlight2" >β-catenin/ZEB1↓, lower levels of nuclear β-catenin in resveratrol treated cells
"highlight2" >MDM2↓, resveratrol activates p53 and suppresses MDM2 levels in colon cancer cells

2687- RES,    Effects of resveratrol, curcumin, berberine and other nutraceuticals on aging, cancer development, cancer stem cells and microRNAs
- Review, NA, NA - Review, AD, NA
"highlight2" >NF-kB↓, RES affects NF-kappaB activity and inhibits cytochrome P450 isoenzyme (CYP A1) drug metabolism and cyclooxygenase activity.
"highlight2" >P450↓,
"highlight2" >COX2↓,
"highlight2" >Hif1a↓, RES may inhibit also the expression of hypoxia-inducible factor-1alpha (HIF-1alpha) and vascular endothelial growth factor (VEGF) and thus may have anti-cancer properties
"highlight2" >VEGF↓,
"highlight2" >*SIRT1↑, RES induces sirtuins, a class of proteins involved in regulation of gene expression. RES is also considered to be a SIRT1-activating compound (STACs).
"highlight2" >SIRT1↓, In contrast, decreased levels of SIRT1 and SIRT2 were observed after treatment of BJ cells with concentrations of RES
"highlight2" >SIRT2↓,
"highlight2" >ChemoSen⇅, However, the effects of RES remain controversial as it has been reported to increase as well as decrease the effects of chemotherapy.
"highlight2" >cardioP↑, RES has been shown to protect against doxorubicin-induced cardiotoxicity via restoration of SIRT1
"highlight2" >*memory↑, RES has been shown to inhibit memory loss and mood dysfunction which can occur during aging.
"highlight2" >*angioG↑, RES supplementation resulted in improved learning in the rats. This has been associated with increased angiogenesis and decreased astrocytic hypertrophy and decreased microglial activation in the hippocampus.
"highlight2" >*neuroP↑, RES may have neuroprotective roles in AD and may improve memory function in dementia.
"highlight2" >STAT3↓, RES was determined to inhibit STAT3, induce apoptosis, suppress the stemness gene signature and induced differentiation.
"highlight2" >CSCs↓,
"highlight2" >RadioS↑, synergistically increased radiosensitivity. RES treatment suppressed repair of radiation-induced DNA damage
"highlight2" >Nestin↓, RES decreased NESTIN
"highlight2" >Nanog↓, RES was determined to suppress the expression of NANOG
"highlight2" >TP53↑, RES treatment activated TP53 and p21Cip1.
"highlight2" >P21↑,
"highlight2" >CXCR4↓, RES downregulated nuclear localization and activity of NF-kappa-B which resulted in decreased expression of MMP9 and C-X-C chemokine receptor type 4 (CXCR4), two proteins associated with metastasis.
"highlight2" >*BioAv↓, The pharmacological properties of RES can be enhanced by nanoencapsulation. Normally the solubility and stability of RES is poor.
"highlight2" >EMT↓, RES was determined to suppress many gene products associated with EMT such as decreased vimentin and SLUG expression but increased E-cadherin expression.
"highlight2" >Vim↓,
"highlight2" >Slug↓,
"highlight2" >E-cadherin↑,
"highlight2" >AMPK↑, RES can induce AMPK which results in inhibition of the drug transporter MDR1 in oxaliplatin-resistant (L-OHP) HCT116/L-OHP CRCs.
"highlight2" >MDR1↓,
"highlight2" >DNAdam↑, RES induced double strand DNA breaks by interfering with type II topoisomerase.
"highlight2" >TOP2↓, The DNA damage was determined to be due to type II topoisomerase poisoning.
"highlight2" >PTEN↑, RES was determined to upregulate phosphatase and tensin homolog (PTEN) expression and decrease the expression of activated Akt.
"highlight2" >Akt↓,
"highlight2" >Wnt↓, RES was shown to decrease WNT/beta-catenin pathway activity and the downstream targets c-Myc and MMP-7 in CRC cells.
"highlight2" >β-catenin/ZEB1↓,
"highlight2" >cMyc↓,
"highlight2" >MMP7↓,
"highlight2" >MALAT1↓, RES also decreased the expression of long non-coding metastasis associated lung adenocarcinoma transcript 1 (RNA-MALAT1) in the LoVo and HCT116 CRC cells.
"highlight2" >TCF↓, Treatment of CRC cells with RES resulted in decreased expression of transcription factor 4 (TCF4), which is a critical effector molecule of the WNT/beta-catenin pathway.
"highlight2" >ALDH↓, RES was determined to downregulate ALDH1 and CD44 in HNC-TICs in a dose-dependent fashion.
"highlight2" >CD44↓,
"highlight2" >Shh↓, RES has been determined to decrease IL-6-induced Sonic hedgehog homolog (SHH) signaling in AML.
"highlight2" >IL6↓, RES has been shown to inhibit the secretion of IL-6 and VEGF from A549 lung cancer cells
"highlight2" >VEGF↓,
"highlight2" >eff↑, Combined RES and MET treatment resulted in a synergistic response in terms of decreased TP53, gammaH2AX and P-Chk2 expression. Thus, the combination of RES and MET might suppress some of the aging effects elicited by UVC-induced DNA damage
"highlight2" >HK2↓, RES treatment resulted in a decrease in HK2 and increased mitochondrial-induced apoptosis.
"highlight2" >ROS↑, RES was determined to shut off the metabolic shift and increase ROS levels and depolarized mitochondrial membranes.
"highlight2" >MMP↓,

2650- RES,    Oxidative Stress Inducers in Cancer Therapy: Preclinical and Clinical Evidence
- Review, Var, NA
"highlight2" >ROS↑, Several molecular mechanisms have been proposed for the anticancer activity of resveratrol, including ROS induction
"highlight2" >Dose↝, ROS, the effect of resveratrol appears to be concentration dependent; at low concentrations, it exerts antioxidant effects, whereas at high concentrations (50–100 µM), resveratrol induces ROS production
"highlight2" >NRF2↑, Cheng et al. [27] reported that resveratrol-induced ROS activate the Nrf2 signaling pathway, which subsequently suppresses NAF1 and induces apoptosis in pancreatic cancer cells.
"highlight2" >NAF1↓,
"highlight2" >ChemoSen↑, This also increased their sensitivity to gemcitabine.
"highlight2" >BioAv↓, Despite the promising potential of resveratrol, its unstable pharmacokinetics due to its high metabolism and poor bioavailability limit its clinical application.

2568- RES,    Resveratrol: A Miracle Drug for Vascular Pathologies
- Review, Var, NA
"highlight2" >antiOx↑, a phytochemical well known for its cardioprotective, antioxidant, anti-inflammatory, anti-atherosclerotic properties in vitro and in vivo.
"highlight2" >Inflam↓,
"highlight2" >cardioP↑, phytochemicals exhibit numerous cardioprotective properties with limited side effects

2567- RES,    Neuroprotective Effects of Resveratrol in Ischemic Brain Injury
- Review, Stroke, NA
"highlight2" >*eff↑, The use of resveratrol (RSV) has been shown to markedly decrease brain damage caused by ischemia in numerous studies.
"highlight2" >*neuroP↑, neuroprotective effect of RSV
"highlight2" >*antiOx↑, therapeutic effects have been related to this polyphenol administration as antioxidant [2], anti-inflammatory [3], cardioprotective [4], and anti-carcinogenic [5], among others
"highlight2" >*Inflam↓,
"highlight2" >*cardioP↑,
"highlight2" >*AntiAg↑, RSV could inhibit the platelet activation and aggregation induced by collagen, adenosine diphosphate, and thrombin

2566- RES,    A comprehensive review on the neuroprotective potential of resveratrol in ischemic stroke
- Review, Stroke, NA
"highlight2" >*neuroP↑, comprehensive overview of resveratrol's neuroprotective role in IS
"highlight2" >*NRF2↑, Findings from previous studies suggest that Nrf2 activation can significantly reduce brain injury following IS and lead to better outcomes
"highlight2" >*SIRT1↑, neuroprotective effects by activating nuclear factor erythroid 2-related factor 2 (NRF2) and sirtuin 1 (SIRT1) pathways.
"highlight2" >*PGC-1α↑, IRT1 activation by resveratrol triggers the deacetylation and activation of downstream targets like peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC-1α) and forkhead box protein O (FOXO)
"highlight2" >*FOXO↑,
"highlight2" >*HO-1↑, ctivation of NRF2 through resveratrol enhances the expression of antioxidant enzymes, like heme oxygenase-1 (HO-1) and NAD(P)H quinone oxidoreductase 1 (NQO1), which neutralize reactive oxygen species and mitigate oxidative stress in the ischemic bra
"highlight2" >*NQO1↑,
"highlight2" >*ROS↓,
"highlight2" >*BP↓, Multiple studies have demonstrated that resveratrol presented protective effects in IS, it can mediate blood pressure and lipid profiles which are the main key factors in managing and preventing stroke
"highlight2" >*BioAv↓, The residual quantity of resveratrol undergoes metabolism, with the maximum reported concentration of free resveratrol being 1.7–1.9 %
"highlight2" >*Half-Life↝, The levels of resveratrol peak 60 min following ingestion. Another study found that within 6 h, there was a further rise in resveratrol levels. This increase can be attributed to intestinal recirculation of metabolites
"highlight2" >*AMPK↑, Resveratrol also increases AMPK and inhibits GSK-3β (glycogen synthase kinase 3 beta) activity in astrocytes, which release energy, makes ATP available to neurons and reduces ROS
"highlight2" >*GSK‐3β↓,
"highlight2" >*eff↑, Furthermore, oligodendrocyte survival is boosted by resveratrol, which may help to preserve brain homeostasis following a stroke
"highlight2" >*AntiAg↑, resveratrol may suppress platelet activation and aggregation caused by collagen, adenosine diphosphate, and thrombin
"highlight2" >*BBB↓, Although resveratrol is a highly hydrophobic molecule, it is exceedingly difficult to penetrate a membrane like the BBB. However, an alternate administration is through the nasal cavity in the olfactory area, which results in a more pleasant route
"highlight2" >*Inflam↓, Resveratrol's anti-inflammatory effects have been demonstrated in many studies
"highlight2" >*MPO↓, Resveratrol dramatically lowered the amounts of cerebral infarcts, neuronal damage, MPO activity, and evans blue (EB) content in addition to neurological impairment scores.
"highlight2" >*TLR4↓, TLR4, NF-κB p65, COX-2, MMP-9, TNF-α, and IL-1β all had greater levels of expression after cerebral ischemia, whereas resveratrol decreased these amounts
"highlight2" >*NF-kB↓,
"highlight2" >*p65↓,
"highlight2" >*MMP9↓,
"highlight2" >*TNF-α↓,
"highlight2" >*IL1β↓,
"highlight2" >*PPARγ↑, Previous studies have shown that resveratrol activates the PPAR -γ coactivator 1α (PGC-1 α), which has free radical scavenging properties
"highlight2" >*MMP↑, Resveratrol can prevent mitochondrial membrane depolarization, preserve adenosine triphosphate (ATP) production, and inhibit the release of cytochrome c
"highlight2" >*ATP↑,
"highlight2" >*Cyt‑c∅,
"highlight2" >*mt-lipid-P↓, mitochondrial lipid peroxidation (LPO), protein carbonyl, and intracellular hydrogen peroxide (H2O2) content were significantly reduced in the resveratrol treatment group, while the expression of HSP70 and metallothionein were restored
"highlight2" >*H2O2↓,
"highlight2" >*HSP70/HSPA5↝,
"highlight2" >*Mets↝,
"highlight2" >*eff↑, Shin et al. showed that 5 mg/kg intravenous (IV) resveratrol reduced infarction volume by 36 % in an MCAO mouse model.
"highlight2" >*eff↑, This study indicates that resveratrol holds the potential to improve stroke outcomes before ischemia as a pre-treatment strategy
"highlight2" >*motorD↑, resveratrol treatment significantly reduced infarct volume and prevented motor impairment, increased glutathione, and decreased MDA levels compared to the control group,
"highlight2" >*MDA↓,
"highlight2" >*NADH:NAD↑, Resveratrol treatment significantly enhanced the intracellular NAD+/NADH ratio
"highlight2" >eff↑, Pretreatment with resveratrol (20 or 40 mg/kg) significantly lowered the cerebral edema, infarct volume, lipid peroxidation products, and inflammatory markers
"highlight2" >eff↑, Intraperitoneal administration of resveratrol at a dose of 50 mg/kg reduced cerebral ischemia reperfusion damage, brain edema, and BBB malfunction

2564- RES,    Effect of resveratrol on platelet aggregation by fibrinogen protection
- in-vitro, NA, NA
"highlight2" >AntiAg↑, The degree of platelet adhesion decreased by increasing the resveratrol concentration.
"highlight2" >antiOx↓, but it seems to be related to its antioxidant activity, its ability to inhibit ribonucleotide reductase, DNA polymerase and cyclooxygenase 2 (COX-2)
"highlight2" >COX2↓,

2472- RES,    Resveratrol Restores Sirtuin 1 (SIRT1) Activity and Pyruvate Dehydrogenase Kinase 1 (PDK1) Expression after Hemorrhagic Injury in a Rat Model
- in-vivo, Nor, NA
"highlight2" >*SIRT1↑, However, resveratrol treatment along with resuscitation fluid restored SIRT1 activity.
"highlight2" >*PGC-1α↑, When resveratrol was administered 10 min after the start of resuscitation, the protein level of SIRT1, PGC-1α and c-Myc in the nuclear fraction was restored.
"highlight2" >*cMyc↑,
"highlight2" >*PDK1↓, The experiments demonstrated a significant increase in PDK1 after T-H, which was abolished by resveratrol treatment

2471- RES,    Resveratrol Regulates Glucose and Lipid Metabolism in Diabetic Rats by Inhibition of PDK1/AKT Phosphorylation and HIF-1α Expression
- in-vivo, Diabetic, NA
"highlight2" >*p‑PDK1↓, RSV treatment significantly downregulated the proteins expression of p-PDK1 and p-AKT (P < 0.01) and the levels of HIF-1α (P < 0.05) and GLUT1 (P < 0.01), while significantly upregulating the level of LDLR (P < 0.05).
"highlight2" >*p‑Akt↓,
"highlight2" >*Hif1a↓,
"highlight2" >*GLUT1↓,

2467- RES,    Resveratrol inhibits Ca2+ signals and aggregation of platelets
- in-vitro, Nor, NA
"highlight2" >*AntiAg↑, The results suggest that resveratrol inhibits thrombin-induced platelet aggregation through decreasing Ca2+ release from its stores and inhibiting store-operated Ca2+ influx into platelets.
"highlight2" >Ca+2↓, Pretreatment of platelets with resveratrol (12.5 μM) attenuated the increase in [Ca2+]i in thrombin- or thapsigargin-stimulated platelets

2443- RES,    Health Benefits and Molecular Mechanisms of Resveratrol: A Narrative Review
- Review, Var, NA
"highlight2" >*antiOx↑, Resveratrol has shown strong antioxidant properties in many studies
"highlight2" >*ROS↓,
"highlight2" >*PTEN↑, resveratrol upregulated the phosphatase and tensin homolog (PTEN), which decreased Akt phosphorylation, leading to an upregulation of antioxidant enzyme mRNA levels such as catalase (CAT) and superoxide dismutase (SOD)
"highlight2" >*Akt↓,
"highlight2" >*Catalase↑,
"highlight2" >*SOD↑,
"highlight2" >*ERK↓, modulating antioxidant enzymes through downregulation of extracellular signal-regulated kinase (ERK)
"highlight2" >*GSH↑, thus the levels of antioxidants like glutathione (GSH) increased, and free radicals were directly scavenged
"highlight2" >*AMPK↑, resveratrol activated adenosine monophosphate (AMP)-activated protein kinase (AMPK) to maintain the structural stability of forkhead box O1 (FoxO1)
"highlight2" >*FOXO1↝,
"highlight2" >*RNS↓, Generally, resveratrol protects against oxidative stress mainly by (i) reducing ROS/reactive nitrogen species (RNS) generation; (ii) directly scavenging free radicals; (iii) improving endogenous antioxidant enzymes (e.g., SOD, CAT, and GSH);
"highlight2" >*Catalase↑,
"highlight2" >*cardioP↑, In summary, the cardiovascular protective effects of resveratrol mainly depend on the capabilities of reducing oxidative stress and alleviating inflammation through Nrf2 and/or SIRT1 activation, PI3K/eNOS upregulation, and NF-κB downregulation.
"highlight2" >*PI3K↑,
"highlight2" >*eNOS↑,
"highlight2" >hepatoP↑, Resveratrol has shown its protective impacts on several liver diseases in some studies

2442- RES,    High absorption but very low bioavailability of oral resveratrol in humans
- in-vitro, Nor, NA
"highlight2" >BioAv↝, The absorption of a dietary relevant 25-mg oral dose was at least 70%, with peak plasma levels of resveratrol and metabolites of 491 +/- 90 ng/ml (about 2 microM)
"highlight2" >Half-Life↝, plasma half-life of 9.2 +/- 0.6 h
"highlight2" >BioAv↓, However, only trace amounts of unchanged resveratrol (<5 ng/ml) could be detected in plasma.
"highlight2" >eff↝, Although the systemic bioavailability of resveratrol is very low, accumulation of resveratrol in epithelial cells along the aerodigestive tract and potentially active resveratrol metabolites may still produce cancer-preventive and other effects.

2441- RES,    Anti-Cancer Properties of Resveratrol: A Focus on Its Impact on Mitochondrial Functions
- Review, Var, NA
"highlight2" >*toxicity↓, Although resveratrol at high doses up to 5 g has been reported to be non-toxic [34], in some clinical trials, resveratrol at daily doses of 2.5–5 g induced mild-to-moderate gastrointestinal symptoms [
"highlight2" >*BioAv↝, After an oral dose of 25 mg in healthy human subjects, the concentrations of native resveratrol (40 nM) and total resveratrol (about 2 µM) in plasma suggested significantly greater bioavailability of resveratrol metabolites than native resveratrol
"highlight2" >*Dose↝, The total plasma concentration of resveratrol did not exceed 10 µM following high oral doses of 2–5 g
"highlight2" >*hepatoP↑, hepatoprotective effects
"highlight2" >*neuroP↑, neuroprotective properties
"highlight2" >*AntiAg↑, Resveratrol possesses the ability to impede platelet aggregation
"highlight2" >*COX2↓, suppresses promotion by inhibiting cyclooxygenase-2 activity
"highlight2" >*antiOx↑, It is widely recognized that resveratrol has antioxidant properties at concentrations ranging from 5 to 10 μM.
"highlight2" >*ROS↓, antioxidant properties at concentrations ranging from 5 to 10 μM.
"highlight2" >*ROS↑, pro-oxidant properties when present in doses ranging from 10 to 40 μM
"highlight2" >PI3K↓, It is known that resveratrol suppresses PI3-kinase, AKT, and NF-κB signaling pathways [75] and may affect tumor growth via other mechanisms as well
"highlight2" >Akt↓,
"highlight2" >NF-kB↓,
"highlight2" >Wnt↓, esveratrol inhibited breast cancer stem-like cells in vitro and in vivo by suppressing Wnt/β-catenin signaling pathway
"highlight2" >β-catenin/ZEB1↓,
"highlight2" >NRF2↑, Resveratrol activated the Nrf2 signaling pathway, causing separation of the Nrf2–Keap1 complex [84], leading to enhanced transcription of antioxidant enzymes, such as glutathione peroxidase-2 [85] and heme-oxygenase (HO-1)
"highlight2" >GPx↑,
"highlight2" >HO-1↑,
"highlight2" >BioEnh?, Resveratrol was demonstrated to have an impact on drug bioavailability,
"highlight2" >PTEN↑, Resveratrol could suppress leukemia cell proliferation and induce apoptosis due to increased expression of PTEN
"highlight2" >ChemoSen↑, Resveratrol enhances the sensitivity of cancer cells to chemotherapeutic agents through various mechanisms, such as promoting drug absorption by tumor cells
"highlight2" >eff↑, it can also be used in nanomedicines in combination with various compounds or drugs, such as curcumin [101], quercetin [102], paclitaxel [103], docetaxel [104], 5-fluorouracil [105], and small interfering ribonucleic acids (siRNAs)
"highlight2" >mt-ROS↑, enhancing the oxidative stress within the mitochondria of these cells, leading to cell damage and death.
"highlight2" >Warburg↓, Resveratrol Counteracts Warburg Effect
"highlight2" >Glycolysis↓, demonstrated in several studies that resveratrol inhibits glycolysis through the PI3K/Akt/mTOR signaling pathway in human cancer cells
"highlight2" >GlucoseCon↓, resveratrol reduced glucose uptake by cancer cells due to targeting carrier Glut1
"highlight2" >GLUT1↓,
"highlight2" >lactateProd↓, therefore, less lactate was produced
"highlight2" >HK2↓, Resveratrol (100 µM for 48–72 h) had a negative impact on hexokinase II (HK2)-mediated glycolysis
"highlight2" >EGFR↓, activation of EGFR and downstream kinases Akt and ERK1/2 was observed to diminish upon exposure to resveratrol
"highlight2" >cMyc↓, resveratrol suppressed the expression of leptin and c-Myc while increasing the level of vascular endothelial growth factor.
"highlight2" >ROS↝, it acts as an antioxidant in regular conditions but as a strong pro-oxidant in cancer cells,
"highlight2" >MMPs↓, Main targets of resveratrol in tumor cells. COX-2—cyclooxygenase-2, SIRT-1—sirtuin 1, MMPs—matrix metalloproteinases,
"highlight2" >MMP7↓, Resveratrol was shown to exert an inhibitory effect on the expression of β-catenins and also target genes c-Myc, MMP-7, and survivin in multiple myeloma cells, thus reducing the proliferation, migration, and invasion of cancer cells
"highlight2" >survivin↓,
"highlight2" >TumCP↓,
"highlight2" >TumCMig↓,
"highlight2" >TumCI↓,

2440- RES,    Resveratrol inhibits Hexokinases II mediated glycolysis in non-small cell lung cancer via targeting Akt signaling pathway
- in-vitro, Lung, H460 - in-vivo, Lung, NA - in-vitro, Lung, H1650 - in-vitro, Lung, HCC827
"highlight2" >AntiTum↑, profound anti-tumor effect on human non-small cell lung cancer (NSCLC) via regulation of glycolysis
"highlight2" >Glycolysis↓,
"highlight2" >HK2↓, Resveratrol impaired hexokinase II (HK2)-mediated glycolysis,
"highlight2" >EGFR↓, Exposure to resveratrol decreased EGFR and downstream kinases Akt and ERK1/2 activation
"highlight2" >Akt↓,
"highlight2" >ERK↓,
"highlight2" >GlucoseCon↓, figure 2
"highlight2" >lactateProd↓, figure 2
"highlight2" >TumCG↓, Resveratrol inhibits tumor growth and HK2 expression in a xenograft mouse model
"highlight2" >Ki-67↓, Ki-67 and HK2 were significantly suppressed in the resveratrol treated group compared with the vehicle treated group

2565- RES,    https://onlinelibrary.wiley.com/doi/10.1111/j.1365-2141.2007.06788.x
- in-vitro, NA, NA - in-vivo, NA, NA
"highlight2" >AntiAg↑, Resveratrol (0·15 and 0·25 μmol/l) inhibited collagen-induced platelet activation accompanied by [Ca+2]i mobilization, thromboxane A2 (TxA2) formation, phosphoinositide breakdown, and protein kinase C (PKC) activation.
"highlight2" >TXA2↑,
"highlight2" >PKCδ↑,
"highlight2" >Dose↝, In an in vivo study, resveratrol (5 mg/kg) significantly prolonged platelet plug formation of mice

2439- RES,    By reducing hexokinase 2, resveratrol induces apoptosis in HCC cells addicted to aerobic glycolysis and inhibits tumor growth in mice
- in-vitro, HCC, HCCLM3 - in-vitro, Nor, L02 - in-vitro, HCC, SMMC-7721 cell - in-vitro, HCC, Bel-7402 - in-vitro, HCC, HUH7
"highlight2" >HK2↓, The induction of mitochondrial apoptosis was associated with the decrease of HK2 expression by resveratrol in HCC cells
"highlight2" >ChemoSen↑, In addition, resveratrol enhanced sorafenib induced cell growth inhibition in aerobic glycolytic HCC cells.
"highlight2" >other↑, HCC cell lines show an increased rate of aerobic glycolysis compared to healthy cells.
"highlight2" >Glycolysis↓, resveratrol suppresses aerobic glycolysis in several cancers, including breast and ovarian cancers
"highlight2" >lactateProd↓, Our data showed that resveratrol (20 μM) treatment of HCC-LM3 cells significantly decreased the concentration of lactate in the cell culture
"highlight2" >TumCP↓, Resveratrol inhibits proliferation and induces apoptosis partly by suppressing HCC glycolysis
"highlight2" >Casp3↑, significant upregulation of active caspase-3 and cleaved PARP in HCC-LM3 cells treated with 40 μM of resveratrol
"highlight2" >cl‑PARP↑,
"highlight2" >PKM2↓, dose of 40 μM, resveratrol downregulated the protein expression of PKM2 in HCC-LM3 and Bel-7402 cells

2334- RES,    Glut 1 in Cancer Cells and the Inhibitory Action of Resveratrol as A Potential Therapeutic Strategy
- Review, Var, NA
"highlight2" >GLUT1↓, resveratrol and other natural products as GLUT1 inhibitors
"highlight2" >GlucoseCon↓, Inhibition of Glucose Uptake by Resveratrol
"highlight2" >lactateProd↓, RSV were able to inhibit glucose uptake, lactate production, Akt, and mTOR signaling
"highlight2" >Akt↓,
"highlight2" >mTOR↓,
"highlight2" >Dose↝, results suggest that RSV can behave differently according to the dose used and the cell type and the metabolic state
"highlight2" >SIRT6↑, RSV induces the expression of silent information regulator-6 (SIRT6) in hypopharyngeal carcinoma FaDu cell line
"highlight2" >PKM2↓, observed that RSV down-regulate pyruvate kinase 2 (PKM2) expression by inhibiting mTOR signaling and suppressed cancer metabolism
"highlight2" >HK2↓, RSV showed a decrease in mRNA and protein levels of GLUT1, HK2, PFK1, and PKM2 which finally caused inhibition of aerobic glycolysis in a study of VEGF-angiogenesis in human umbilical vein endothelial cells
"highlight2" >PFK1↓,
"highlight2" >ChemoSen↑, combinatorial strategies that could use GLUT1 inhibitors such as RSV with anticancer conventional drugs for therapy are promising

2331- RES,    Resveratrol improves follicular development of PCOS rats via regulating glycolysis pathway and targeting SIRT1
- in-vivo, Nor, NA
"highlight2" >*LDHA↑, resveratrol treatment significantly increased the expression of LDH-A, PKM2, and SIRT1 in the ovarian tissues of PCOS rats
"highlight2" >*PKM2↑,
"highlight2" >*SIRT1↑,
"highlight2" >*Glycolysis↝, protective effects of resveratrol in the PCOS rats may be associated with the regulation of glycolysis-related mediators including PKM2, LDH-A, and SIRT1.

2333- RES,    Resveratrol regulates insulin resistance to improve the glycolytic pathway by activating SIRT2 in PCOS granulosa cells
- in-vitro, Nor, NA
"highlight2" >*glucose↓, RES played a protective role on the IR in PCOS rats, which significantly decreased the levels of blood glucose and serum insulin, up regulated the expression of IGF1R, and down regulated the expression of IGF1.
"highlight2" >*Insulin↓,
"highlight2" >*IGFR↓,
"highlight2" >*IGF-1↓,
"highlight2" >*LDHA↑, RES overtly repaired the glycolysis process by reversing the levels of lactic acid and pyruvate, together with up regulating the expression level of LDHA, HK2, and PKM2, after AGK2 treatment.
"highlight2" >*HK2↑,
"highlight2" >*PKM2↑,
"highlight2" >*Glycolysis↝, RES could eectively improve insulin resistance and restore the glycolysis pathway by regulating SIRT2, which may contribute to attenuating the ovarian damage of PCOS rat
"highlight2" >*SIRT2↑, activating SIRT2 in PCOS granulosa cells

3034- RosA,  RES,  Ba,    The effect of dietary polyphenols on the epigenetic regulation of gene expression in MCF7 breast cancer cells
- in-vitro, BC, MCF-7
"highlight2" >DNMTs↓, Figure 2B DNMT inhibition weak ~80% of control
"highlight2" >eff↑, Note Resveratrol is stronger at 20% of control
"highlight2" >eff↝, Baicalein also weak at 80% of control

2306- SIL,  CUR,  RES,  EA,    Identification of Natural Compounds as Inhibitors of Pyruvate Kinase M2 for Cancer Treatment
- in-vitro, BC, MDA-MB-231
"highlight2" >PKM2↓, silibinin, curcumin, resveratrol, and ellagic acid as potential inhibitors of PKM2
"highlight2" >Dose↝, IC50 values of 0.91 µM, 1.12 µM, 3.07 µM, and 4.20 µM respectively(enzymatic-assay-based screening)
"highlight2" >Dose↝, IC50 against MDA-MB231 cells 208uM, 26uM, 306uM, 20um respectively

2206- SNP,  RES,    ENHANCED EFFICACY OF RESVERATROL-LOADED SILVER NANOPARTICLE IN ATTENUATING SEPSIS-INDUCED ACUTE LIVER INJURY: MODULATION OF INFLAMMATION, OXIDATIVE STRESS, AND SIRT1 ACTIVATION
- in-vivo, Nor, NA
"highlight2" >*hepatoP↑, AgNPs + RV treatment significantly reduced pro-inflammatory cytokines, NF-κB activation, presepsin, PCT, 8-OHDG, and VEGF levels compared with the CLP group, indicating attenuation of sepsis-induced liver injury.
"highlight2" >*Inflam↓,
"highlight2" >*NF-kB↓,
"highlight2" >*VEGF↓,
"highlight2" >*SIRT1↑, Both RV and AgNPs + RV treatments increased SIRT1 levels, suggesting a potential role of SIRT1 activation in mediating the protective effects.
"highlight2" >*ROS↓, alleviating sepsis-induced liver injury by modulating inflammation, oxidative stress, and endothelial dysfunction, potentially mediated through SIRT1 activation.
"highlight2" >*Dose↝, 30 mg/kg of AgNPs + RV was given intraperitoneally to the rats
"highlight2" >*Catalase↑, AgNPs + RV treatment exhibited a robust effect in bolstering CAT activity
"highlight2" >*MDA↓, AgNPs + RV treatment effectively ameliorates sepsis-induced oxidative stress and inflammation in rat livers by reducing MDA, MPO, and NO levels
"highlight2" >*MPO↓,
"highlight2" >*NO↓,
"highlight2" >*ALAT↓, AgNPs + RV effectively reduced the ALT and AST levels, returning them to values similar to those observed in the Sham group
"highlight2" >*AST↓,
"highlight2" >*antiOx↑, corroborates the antioxidant potential of RV and AgNPs observed in earlier studies

119- UA,  CUR,  RES,    Combinatorial treatment with natural compounds in prostate cancer inhibits prostate tumor growth and leads to key modulations of cancer cell metabolism
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3
"highlight2" >ROS⇅, ROS↑ only with CUR alone, otherwise ↓
"highlight2" >p‑STAT3↓,
"highlight2" >Src↓,
"highlight2" >AMPK↑,

3921- VitD3,  RES,    Vitamin D Combined with Resveratrol Prevents Cognitive Decline in SAMP8 Mice
- in-vivo, AD, NA
"highlight2" >*cognitive↑, The combination of VD and RSV significantly increased time spent in target quadrant and the number of crossing via MWM test
"highlight2" >*Aβ↓, In hippocampus, the combined intervention significantly reduced soluble Aβ42 level and BACE1 protein expression
"highlight2" >*BACE↓,
"highlight2" >*p‑tau↓, combined treatment significantly reduced phosphorylation of tau at serine404 and p-p53, as well as enhanced p-CREB protein expression
"highlight2" >*p‑CREB↑,
"highlight2" >*p‑NF-kB↓, The combination also significantly reduced GFAP and p-NFκB p65 in both hippocampus and cortex
"highlight2" >*neuroP↑, combined intervention might exert greater neuroprotective effects in SAMP8 mice,


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 141

Results for Effect on Cancer/Diseased Cells:
5LO↓,1,   ACTA2↓,1,   AhR↓,1,   Akt↓,11,   p‑Akt↓,1,   ALDH↓,1,   ALDH1A1↓,1,   AMPK↑,4,   angioG↓,8,   AntiAg↑,2,   AntiAge↑,1,   antiOx↓,1,   antiOx↑,1,   AntiTum↑,3,   Apoptosis↑,17,   AR↓,4,   ATF3↑,1,   ATF4↑,1,   ATF6↑,2,   ATM↑,1,   ATP↓,2,   ATP↑,1,   Axin2↓,1,   Aβ↓,1,   BAX↓,1,   BAX↑,7,   Bcl-2↓,9,   Bcl-xL↓,3,   Beclin-1↓,1,   BIM↑,1,   BioAv↓,5,   BioAv↑,3,   BioAv↝,1,   BioEnh?,1,   BMP2↑,1,   BNIP3↑,1,   BRCA1↑,1,   Ca+2↓,1,   Ca+2↑,3,   Ca+2↝,1,   cardioP↑,2,   Casp3↑,8,   cl‑Casp3↑,1,   Casp9↑,4,   Catalase↓,1,   CD133↓,1,   CD24↓,1,   CD4+↓,1,   CD44↓,2,   CD8+↑,1,   CDK2↓,1,   CDK4↓,1,   CDK4↝,1,   CDK6↓,1,   cellSen↑,1,   chemoP↑,2,   ChemoSen↑,13,   ChemoSen⇅,1,   ChemoSideEff↓,1,   p‑CHK1↑,1,   CHOP↑,4,   cJun↑,1,   CK2↓,3,   cMyc↓,5,   COX2↓,11,   CRP↓,1,   CSCs↓,4,   CXCL12↓,1,   CXCR2↑,1,   CXCR4↓,2,   cycA1↑,1,   CycB↓,1,   cycD1↓,8,   cycD1↑,1,   cycE↑,1,   Cyt‑c↑,4,   Diablo↑,1,   DNAdam↓,1,   DNAdam↑,3,   DNMTs↓,2,   Dose?,1,   Dose↑,2,   Dose↝,9,   DR4↑,2,   DR5↑,2,   E-cadherin↓,2,   E-cadherin↑,6,   E6↓,1,   ECAR↓,1,   eff↓,3,   eff↑,17,   eff↝,3,   EGFR↓,3,   p‑eIF2α↑,2,   EMT↓,11,   EP4↑,1,   ER Stress↑,5,   ERK↓,3,   p‑ERK↓,1,   EZH2↓,1,   FAK↓,2,   FasL↓,1,   FASN↑,1,   FBI-1↓,1,   FDG↓,1,   Ferroptosis↑,1,   FGF↑,1,   Fibronectin↓,1,   Fibronectin↑,1,   FOXO↑,2,   FOXO4↓,1,   FOXP3↓,1,   G6PD↓,1,   GADD34↑,1,   Gli1↓,3,   GlucoseCon↓,6,   GLUT1↓,4,   GlutMet↓,1,   Glycolysis↓,6,   GPx↑,1,   GPx4↓,1,   GRP78/BiP↑,2,   GRP94↑,1,   GSH↓,1,   GSK‐3β↑,1,   GSK‐3β↝,1,   H2O2↑,1,   Half-Life↓,1,   Half-Life↑,1,   Half-Life↝,3,   HDAC↓,3,   HDAC1↓,1,   HDAC3↓,1,   HDAC8↓,1,   hepatoP↑,1,   HH↓,3,   Hif1a↓,12,   Hif1a↑,1,   HK2↓,6,   HLA↑,1,   HO-1↓,1,   HO-1↑,2,   HSP27↓,1,   IGF-1↓,2,   IGF-1R↓,1,   IL1↓,1,   IL10↓,1,   IL18↓,1,   IL1β↓,2,   IL6↓,6,   IL8↓,2,   Inflam↓,3,   iNOS↓,1,   IRE1↑,1,   ITGB1↓,1,   JAK↓,1,   JAK2↓,1,   p‑JNK↓,2,   Ki-67↓,3,   lactateProd↓,7,   LDH↓,1,   lipid-P↓,2,   lipid-P↑,1,   Macrophages↓,1,   MALAT1↓,3,   MAPK↓,2,   MAPK↑,2,   Mcl-1↓,2,   MCP1↓,1,   MDM2↓,1,   MDR1↓,1,   miR-21↓,1,   miR-27a-3p↓,1,   MKP5↑,1,   MMP↓,7,   MMP2↓,7,   MMP7↓,2,   MMP9↓,12,   MMPs↓,4,   mTOR↓,7,   N-cadherin↓,3,   N-cadherin↑,1,   NA↓,1,   NADPH↑,1,   NAF1↓,3,   Nanog↓,2,   necrosis↑,1,   Nestin↓,1,   Neut↓,1,   NF-kB↓,13,   p‑NF-kB↓,2,   NKG2D↑,1,   NLRP3↓,5,   NOTCH⇅,1,   NOTCH1↓,1,   NOTCH2↓,1,   NOTCH2↑,1,   NRF2↓,1,   NRF2↑,7,   OCR↑,1,   OCT4↓,1,   other↓,3,   other↑,1,   OXPHOS↓,1,   OXPHOS↑,1,   P21↓,1,   P21↑,5,   p27↓,1,   p27↑,5,   p300↓,1,   p38↓,1,   p38↑,1,   p‑p38↑,2,   P450↓,1,   P53↑,9,   p53 Wildtype∅,1,   p62↓,2,   p62↑,1,   p65↓,1,   PARP↑,1,   p‑PARP↑,1,   cl‑PARP↑,2,   cl‑PARP1↑,1,   PD-1↓,1,   PD-L1↑,1,   PDGFR-BB↓,1,   PDH↑,2,   PERK↑,2,   PFK↓,2,   PFK1↓,2,   PGE2↓,1,   PI3K↓,5,   p‑PI3K↓,1,   PI3K/Akt↓,1,   PKCδ↑,1,   PKM2↓,7,   POLD1↓,1,   PPP↓,1,   Prx↓,1,   PSA↓,2,   PTCH1↓,2,   PTEN↑,4,   PUMA↑,1,   R5P↝,1,   RadioS↑,6,   RAS↓,1,   Rho↓,1,   ROCK1↓,2,   ROS↓,3,   ROS↑,24,   ROS⇅,1,   ROS↝,1,   mt-ROS↑,1,   selectivity↑,1,   Shh↓,1,   SIRT1↓,1,   SIRT1↑,12,   SIRT2↓,1,   SIRT3↑,1,   SIRT6↑,1,   Slug↓,3,   SMAD2↓,2,   p‑SMAD2↓,1,   SMAD3↓,2,   p‑SMAD3↓,1,   Smo↓,2,   Snail↓,3,   Snail↑,1,   SOD2↓,1,   SOX2↓,2,   SOX9↑,1,   Sp1/3/4↓,8,   Sp1/3/4↑,1,   Src↓,1,   STAT3↓,7,   p‑STAT3↓,1,   STAT5↓,1,   survivin↓,7,   T-Cell↓,1,   T-Cell↑,2,   TAC?,1,   talin↓,1,   TCF↓,2,   Telomerase↓,1,   TET1↑,2,   TGF-β↓,3,   Th1 response↑,1,   TIMP1↑,2,   TIMP2↑,2,   TIMP3↑,1,   TKT↝,1,   TNF-α↓,3,   TOP1?,1,   TOP2↓,1,   TP53↑,1,   Trx↓,1,   Trx1↓,1,   TumAuto↓,1,   TumAuto↑,2,   TumCCA↑,11,   TumCD↑,1,   TumCG↓,7,   TumCI↓,11,   TumCMig↓,8,   TumCP↓,15,   tumCV↓,5,   TumMeta↓,5,   TumVol↓,1,   TumW↓,1,   TXA2↑,1,   uPA↓,1,   uPAR↓,1,   UPR↑,2,   VEGF↓,9,   Vim?,1,   Vim↓,3,   Vim↑,1,   Warburg↓,2,   Wnt↓,6,   Wnt/(β-catenin)↓,1,   XBP-1↑,1,   xCT↓,1,   XIAP↓,2,   YAP/TEAD↓,1,   ZBTB10↑,1,   Zeb1↓,2,   α-SMA↓,2,   β-catenin/ZEB1↓,5,   γH2AX↑,3,  
Total Targets: 329

Results for Effect on Normal Cells:
Acetyl-CoA↓,1,   AChE↓,1,   ADAM10↑,6,   Akt↓,1,   Akt↑,1,   p‑Akt↓,1,   ALAT↓,1,   AMPK↑,10,   angioG↑,1,   AntiAg↑,6,   AntiCan↑,1,   antiOx↑,18,   Apoptosis↓,2,   AST↓,1,   ATP↑,1,   Aβ↓,8,   BACE↓,3,   BAX↓,1,   BBB↓,1,   BBB↑,1,   Bcl-2↑,1,   BDNF↑,4,   Beclin-1↑,1,   BioAv↓,7,   BioAv↑,5,   BioAv↝,2,   BioEnh↑,1,   BP↓,1,   CaMKII ↓,1,   cardioP↑,6,   Casp3↓,1,   Catalase↑,6,   chemoP↑,2,   cMyc↑,1,   cognitive↑,6,   COX2↓,4,   p‑CREB↑,2,   Cyt‑c∅,1,   Dose↓,1,   Dose↝,2,   ECAR∅,1,   eff↑,4,   eNOS↑,1,   ERK↓,1,   FAO↑,1,   FASN↓,1,   FOXO↑,1,   FOXO1↝,1,   G6PD↑,1,   glucose↓,1,   GLUT1↓,1,   GlutMet↑,1,   Glycolysis↝,2,   GPx↑,5,   GSH↑,9,   GSK‐3β↓,3,   GSK‐3β↑,1,   GSR↑,1,   GSTs↑,1,   H2O2↓,1,   Half-Life↓,2,   Half-Life↝,1,   hepatoP↑,3,   Hif1a↓,1,   HK2↑,1,   HO-1↑,9,   HO-1⇅,1,   HSP70/HSPA5↝,1,   IGF-1↓,2,   IGFBP3↑,1,   IGFR↓,1,   IL1β↓,4,   IL6↓,2,   Inflam↓,13,   iNOS↓,2,   iNOS↑,1,   Insulin↓,1,   Keap1↓,3,   LDHA↑,2,   LDL↓,1,   lipid-P↓,5,   mt-lipid-P↓,1,   MDA↓,4,   memory↑,7,   Mets↝,1,   miR-155↓,1,   miR-29b↑,1,   MMP↑,2,   MMP3↓,1,   MMP9↓,5,   motorD↑,1,   MPO↓,2,   mtDam↓,1,   NADH:NAD↑,1,   neuroP↑,17,   NF-kB↓,6,   NF-kB↑,1,   p‑NF-kB↓,1,   NLRP3↓,4,   NO↓,2,   NQO1↑,2,   Nrf1?,1,   NRF2↑,9,   OS↑,1,   other?,1,   other↑,2,   P21↑,1,   p38↑,1,   p62↓,1,   p65↓,1,   PDK1↓,1,   p‑PDK1↓,1,   PGC-1α↓,1,   PGC-1α↑,2,   PGE2↓,1,   PI3K↑,2,   PKA↑,1,   PKM2↑,2,   PP2A↑,4,   PPARγ↑,2,   PSD95↑,1,   PTEN↑,1,   radioP↑,1,   RenoP↑,2,   RNS↓,1,   ROS↓,19,   ROS↑,1,   SIRT1↑,18,   SIRT2↑,1,   SOD↑,6,   Sp1/3/4↓,3,   Sp1/3/4↑,1,   SREBP1↓,1,   tau↓,1,   p‑tau↓,6,   TLR4↓,1,   TNF-α↓,2,   toxicity↓,3,   toxicity↑,1,   toxicity∅,1,   VEGF↓,1,   VEGF↑,1,   Weight↑,1,  
Total Targets: 143

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:141  Target#:%  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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