other Cancer Research Results
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Scientific Papers found: Click to Expand⟱
ROS↑, selectively enhancing metabolic oxidative stress.
GlucoseCon↓, mimic in vitro glucose deprivation that selectively kills cancer cells by oxidative stress.
other↓, Treatment with antioxidants protects neuroblastoma cells from 2DG-induced cell killing
ChemoSen↑, combination of 2DG and cisplatin resulted in a significant decrease in cell survival when compared with 2DG or cisplatin alone
ROS↑,
GSH↓,
other↓, Simultaneous treatment with the thiol antioxidant N-acetylcysteine (NAC) inhibited parameters indicative of oxidative stress, as well as protected FaDu cells from the cytotoxic effects of cisplatin alone and the combination of 2DG and cisplatin.
*other↑, Low glycemic index foods seem to improve attention, memory and functional capacity, while those rich in simple sugars are associated with difficulty in concentration and attention.
*other↓, Low levels of serotonin have been linked to decreased learning, reasoning and memory.
*cognitive↑, It is advisable to consume diets with an adequate ratio (5:1) of omega-6: 3 fatty acids (Mediterranean diet) given that they are associated with better memory capacity and lower risk of cognitive deterioration.
*eff↑, Vitamins B1, B6, B12, B9 (folic acid) and D, choline, iron and iodine exert neuroprotective effects and improve intellectual performance.
*eff↑, In parallel, antioxidants (vitamins C, E, A, zinc, selenium, lutein and zeaxanthin) have a very important role in the defense against oxidative stress associated with mental deterioration and in the improvement of cognition.
other↓, Combined STM2457 and APS treatment significantly reduced m6A levels, METTL3, HNRNPA2B1, and FOXQ1 expression, and mRNA stability compared to single-drug treatments, approaching or surpassing METTL3 silencing effects.
TumCP↓, The combination markedly suppressed cell proliferation, migration, invasion, and EMT, with increased E-cadherin and decreased N-cadherin levels.
TumCMig↓,
TumCI↓,
EMT↓,
E-cadherin↑,
N-cadherin↓,
TumCG↓, In vivo, combination therapy significantly reduced tumor growth and FOXQ1 expression, outperforming single-drug treatments.
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in-vitro, |
BC, |
MCF-7 |
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in-vitro, |
BC, |
T47D |
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in-vitro, |
BC, |
MDA-MB-231 |
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TumCD↑, AgNPs showed potent cytotoxicity in breast cancer cells, no matter whether they were tamoxifen sensitive or resistant.
other↓, Next, we found that a long noncoding RNA, XLOC_006390, was decreased in AgNPs-treated breast cancer cells, coupled to inhibited cell proliferation, altered cell cycle and apoptotic phenotype.
P53↑, According to the literature, AgNPs may induce cancer cells apoptosis by activating p53, so as to achieve the antitumor effect
TumCCA↑, We found that AgNPs treatment at 150 μg/ml could induce G0/G1 cell cycle arrest
Apoptosis↑, and promote both early apoptosis and late apoptosis/necrosis rate
ChemoSen↑, AgNPs-based approaches provided a potential way to fight drug resistance and reduce the toxicity related to chemotherapy drugs
tumCV↓, One of the highlights of this study is that AgNPs have strong cytotoxicities on all the breast cancer cell lines and clinically isolated breast cancer cells, with the IC50s at about 150 μg/ml for all
γH2AX↑, early apoptosis markers (γH2AX), was also significantly upregulated by AgNPs treatment
SOX4↓, AgNPs can inhibit the SOX4 expression by regulating XLOC_006390/miR-338-3p axis.
other↓, Akk diminished in both humans and mice with lung cancer
other↓, heating destroyed garlic's active allyl sulfur compound formation, which may relate to its anticancer properties
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Review, |
BC, |
SkBr3 |
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Review, |
neuroblastoma, |
SK-N-SH |
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Review, |
AD, |
NA |
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PDH↑, ALA is capable of activating pyruvate dehydrogenase in tumor cells.
TumCG↓, ALA also significantly inhibited tumor growth in mouse xenograft model using BCPAP and FTC-133 cells
ROS↑, ALA is able to generate ROS, which promote ALA-dependent cell death in lung cancer [75], breast cancer [76] and colon cancer
AMPK↑,
EGR4↓,
Half-Life↓, Data suggests that ALA has a short half-life and bioavailability (about 30%)
BioAv↝,
*GSH↑, Moreover, it is able to increase the glutathione levels inside the cells, that chelate and excrete a wide variety of toxins, especially toxic metals from the body
*IronCh↑, The existence of thiol groups in ALA is responsible for its metal chelating abilities [14,35].
*ROS↓, ALA exerts a direct impact in oxidative stress reduction
*antiOx↑, ALA is being referred as the universal antioxidant
*neuroP↑, ALA has neuroprotective effects on Aβ-mediated cytotoxicity
*Ach↑, ALA show anti-dementia or anti-AD properties by increasing acetylcholine (ACh) production through activation of choline acetyltransferase, which increases glucose absorption
*lipid-P↓, ALA has multiple and complex effects in this way, namely scavenging ROS, transition metal ions, increasing the levels of reduced glutathione [59,63], scavenging of lipid peroxidation products
*IL1β↓, ALA downregulated the levels of the inflammatory cytokines IL-1B and IL-6 in SK-N-BE human neuroblastoma cells
*IL6↓,
TumCP↓, ALA inhibited cell proliferation, [18F]-FDG uptake and lactate formation and increased apoptosis in neuroblastoma cell lines Kelly, SK-N-SH, Neuro-2a and in the breast cancer cell line SkBr3.
FDG↓,
Apoptosis↑,
AMPK↑, ALA suppressed thyroid cancer cell proliferation and growth through activation of AMPK and subsequent down-regulation of mTOR-S6 signaling pathway in BCPAP, HTH-83, CAL-62 and FTC-133 cells lines.
mTOR↓,
EGFR↓, ALA inhibited cell proliferation through Grb2-mediated EGFR down-regulation
TumCI↓, ALA inhibited metastatic breast cancer cells migration and invasion, partly through ERK1/2 and AKT signaling
TumCMig↓,
*memory↑, Alzheimer’s Disease: ALA led to a marked improvement in learning and memory retention
*BioAv↑, Since ALA is poorly soluble, lecithin has been used as an amphiphilic matrix to enhance its bioavailability.
*BioAv↝, ALA were found to be considerably higher in adults with mean age greater than 75 years as compared to young adults between the ages of 18 and 45 years.
*other↓, ALA treatment has been recently studied by some clinical trials to explain its efficacy in preventing miscarriage
*other↝, 1800 mg of ALA or placebo were administrated orally every day, except during the period 2 days before to 4 days after administration of each dose of platinum to avoid potential interference with platinum’s antitumor effects
*Half-Life↓, Data shows a short half-life and bioavailability of about 30% of ALA due to mechanisms involving hepatic degradation, reduced ALA solubility as well as instability in the stomach.
*BioAv↑, ALA bioavailability is greatly reduced after food intake and it has been recommended that ALA should be admitted at least 2 h after eating or if taken before; meal should be taken at least 30 min after ALA administration
*ChAT↑, ALA show anti-dementia or anti-AD properties by increasing acetylcholine (ACh) production through activation of choline acetyltransferase, which increases glucose absorption
*GlucoseCon↑,
*BChE↓, Essential oils (EOs) from Salvia leriifolia Benth. exhibited high BChE inhibitory.
*AChE↓, Volatile oil from Marlierea racemosa Vell. (Myrtaceae) demonstrated concentration‐dependent inhibition of AChE
*other↓, EOs from the leaves and flowers of Polygonum hydropiper L., 28 sandalwood oil and its chief constituent α‐santalol were reported the AChE, BChE inhibitory efficacy.
*other?, The extract of Rosmarinus officinalis L. leaf led to improved long‐term memory in scopolamine‐induced rats, which can be partially explained by its inhibition of AChE activity in rat brain
*Ach?, It was observed in APP/PS1 mice that 4 weeks of Lemon essential oil treatment could significantly decrease hippocampal AChE, and thus increased ACh levels
*eff↑, Most studies have found that terpenoids in aromatic plant extracts are the main anticholinesterase active components
*antiOx↑, aromatic plant extracts for their potent antioxident and free radical scavenging properties
*ROS↓, Several compounds like safranal, linalool, and SHXW essential oil have been found to decrease ROS levels induced by Aβ in rats or mouse
*cognitive↑, aromatic plant extracts can improve cognitive function, reduce agitation, and improve sleep quality in AD patients.
*Mood↑,
*Sleep↑,
*cognitive↑, EOs were effective on several pathological targets and have improved cognitive performance in animal models and human subjects.
*AChE↓, Recently, Ayaz et al. (2015) reported the AChE, BChE inhibitory and free radicals scavenging efficacy of EOs from the leaves and flowers of Polygonum hydropiper.
*BChE↓,
*ROS↓,
*other↓, , Ahmad et al. (2016) reported the anti-cholinesterase and antiradicals potentials of EO from Rumex hastatus D. Don. GC-MS analysis of EO revealed the presence of 123 compounds. I
*other↓, (Ahmad et al., 2016). Okello et al. (2008) reported the in vitro AChE, BChE inhibitory activity of flower oil from Narcissus poeticus L. belonging to family Amaryllidaceae.
*other↓, The EO from Marlierea racemosa Vell. (Myrtaceae) were evaluated by Souza et al. (2009) against AChE enzyme.
*other↓, C. salvifolius exhibited AChE inhibitory activity with IC50 value of 58.1 μg/ml. Whereas, C. libanotis, C. creticus and C. salvifolius showed significant inhibitory activities against BChE with IC50 values of 23.7, 29.1 and 34.2 μg/ml respectively.
*other↓, Rosemary EO also possess moderate AChE inhibitory activity and can synergistically act with 2-pinene and 1,8-cineole.
*memory↑, Owing to the memory enhancing capabilities of Salvia lavandulifolia Vahl (Spanish sage),
*BACE↓, EOs can inhibit the activity of BACE1 to hamper the Aβ load.
*Mood↑, Lavandula angustifolia Mill. and Melissa officinalis L. belonging to Lamiaceae for the management of agitation in individuals with severe dementia. The sedative and calming effect of both EOs is already established which can contribute in consolidati
*motorD↑, lavender EO: locomotor activity and motor functions were improved in animal models.
*cognitive↑, Aromatherapy may have some potential for improving cognitive function, especially in AD patients.
*other↑, Lavandula angustifolia Mill, Salvia rosmarinus and lemon citrus:potential for improving cognitive function, especially in AD patients.
*other↓, Rosmarinus officinalis: improving cognitive function by inhaled administration
*BioAv↑, There is no doubt that components from EOs are often absorbed through the skin, enter into the circulation then
cross the BBB.
*BBB?,
AntiCan↑, Artemisinin is an anti-malarial drug that has shown anticancer properties
Ferroptosis↑, Recently, ferroptosis was reported to be induced by dihydroartemisinin (DHA) and linked to iron increase.
Iron↑, We found that treatment of DHA induces early ferroptosis by promoting ferritinophagy and subsequent iron increase.
Mets↑, Furthermore, our study demonstrated that DHA activated zinc metabolism signaling, especially the upregulation of metallothionein (MT).
eff↑, Supportingly, we showed that inhibition MT2A and MT1M isoforms enhanced DHA-induced ferroptosis.
GSH↝, Finally, we demonstrated that DHA-induced ferroptosis alters glutathione pool, which is highly dependent on MTs-driven antioxidant response.
eff↑, DHA cooperates with FAC to increase the intracellular iron pool. ferric citrate iron (FAC)
other↓, Under oxidative stress, MT can release Zn2+ (apo-MT) to form thiol groups and participates in GSSG/ GSH reduction.
eff↑, Our current findings also suggest that MT chemical inhibition can cooperate with DHA in primary AML cells in patients.
other↓, Subsequent MT inhibition may sensitize leukemic cells to lipid peroxidation in vitro by impairing GSH regeneration.
Risk↓, Meta-analyses of 118 observational studies of mortality in cancer patients give evidence consistent with reductions of about 20% in mortality associated with aspirin use.
*toxicity↓, Reasons against aspirin use include increased risk of a gastrointestinal bleed though there appears to be no valid evidence that aspirin is responsible for fatal gastrointestinal bleeding.
other↑, In conclusion, given the relative safety and the favourable effects of aspirin, its use in cancer seems justified, and ethical implications of this imply that cancer patients should be informed of the present evidence
*COX1↓, recent evidence highlights additional targets for aspirin in tackling cancer progression directly, irrespective of COX activity [3, 4]
TumCP↓, Such targets include energy metabolism involved in cancer proliferation, cancer associated inflammation [5] and platelet driven pro-carcinogenic activity [2].
DNArepair↑, beneficial effect of aspirin on colon cancer risk through an enhancement of DNA-repair mechanisms [2].
ChemoSen↑, ‘basic science’ basis to justify using aspirin as an adjunct to other pre-existing therapies (e.g., immunotherapy and cytotoxic chemotherapy) in the treatment of cancer progression and metastasis [2, 14].
other↓, Aspirin has been shown repeatedly to reduce thromboembolism, including in patients with cancer [15]
Risk↓, Current use of aspirin vs never use was associated with lower CRC risk (hazard ratio [HR] 0.87, 95% confidence interval
other↝, However, some large cohorts found no association between aspirin use and CRC risk when aspirin was initiated after 70 years of age (9) and when aspirin was used for less than 10 years (10) or 20 years (11).
Dose↝, Use of 160 mg tablets was associated with a greater CRC risk reduction than the use of 75 mg tablets.
Risk↓, We found a 13% lower CRC risk associated with current low-dose aspirin use vs never use,
other↓, In 2020, a large meta-analysis of 15 cohort, 11 nested case-control, and 19 case-control studies reported a 27% reduced CRC risk in regular users of aspirin (7)
other↝, It was argued later that the limited follow-up time of participants without history of aspirin use before the trial enrollment could partly explain the negative results in the ASPREE trial (9,36).
KRAS↓, A mechanism supporting the hypothesis that aspirin has a protective effect against CRC risk is that aspirin blocks the mutated APC (adenomatous polyposis coli) gene, leading to the inhibition of the KRAS pathway and the adenomatous polyp formation (3
other↓, By assuming a protective effect of aspirin against CRC, we estimated that 1,073 cases with CRC were prevented by aspirin use, equating to 2.7% lower CRC incidence.
other↓, In conclusion, our study provided novel and strong evidence that low-dose aspirin use is associated with a lower CRC risk.
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BC, |
MDA-MB-231 |
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BC, |
MCF-7 |
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in-vitro, |
Nor, |
HMEC |
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eff↑, WA treatment caused ROS production in MDA-MB-231 and MCF-7 cells, but not in a normal human mammary epithelial cell line (HMEC). ****
mt-ROS↑, WA-induced apoptosis in human breast cancer cells is mediated by mitochondria-derived ROS
mitResp↓,
OXPHOS↓, WA exposure was accompanied by inhibition of oxidative phosphorylation and inhibition of complex III activity.
compIII↑,
BAX↑,
Bak↑,
other↓, Cu,Zn-Superoxide dismutase (Cu,Zn-SOD) overexpression confers protection against WA-induced ROS production and apoptosis
ATP∅, steady-state levels of ATP were unaffected by WA treatment in either cell line
*ROS∅, but not in a normal human mammary epithelial cell line (HMEC). WA treatment caused ROS production in breast cancer cells, HMEC were resistant to pro-oxidant effect of this agent.
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Review, |
Nor, |
NA |
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Review, |
IBD, |
NA |
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Review, |
Diabetic, |
NA |
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*Wound Healing↑, Traditionally recognized for its anti-inflammatory and antimicrobial effects, which are very important in wound healing, the Aloe Vera relies on its polysaccharides
*Imm↑, which confer immunomodulatory, antioxidant, and tissue-regenerative properties.
*antiOx↑,
*AntiDiabetic↑, graphical abstract
*AntiCan↑,
*Inflam↓, The anti-inflammatory properties of Aloe Vera polysaccharides are primarily mediated through the inhibition of key inflammatory pathways.
*NF-kB↓, Acemannan and other polysaccharides suppress the activation of nuclear factor-kappa B (NF-κB), a transcription factor that regulates the expression of pro-inflammatory genes.
*COX2↓, By inhibiting NF-κB [48,49], Aloe Vera polysaccharides reduce the production of cyclooxygenase-2 (COX-2) and lipoxygenase (LOX),
*5LO↓,
*IL1β↓, Aloe Vera polysaccharides downregulate the expression of pro-inflammatory cytokines like IL-1β, IL-6, and TNF-α, while upregulating anti-inflammatory cytokines such as IL-10
*IL6↓,
*TNF-α↓,
*IL10↑,
*other↓, This dual action helps to mitigate inflammation in conditions such as arthritis, dermatitis, and inflammatory bowel disease (IBD)
*ROS↓, Aloe Vera polysaccharides exhibit potent antioxidant activity by scavenging reactive oxygen species (ROS) and free radicals,
*SOD↑, The polysaccharides enhance the activity of endogenous antioxidant enzymes, such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), which neutralize oxidative stress and protect cells from damage [17,63].
*Catalase↑,
*GPx↑,
*lipid-P↓, This property is particularly beneficial in preventing lipid peroxidation, DNA damage, and protein oxidation, processes associated with chronic diseases and aging
*DNAdam↓,
*GutMicro↑, Aloe Vera polysaccharides support gastrointestinal health, acting as prebiotics and promoting the growth of beneficial gut microbiota such as Lactobacillus and Bifidobacterium species [64].
*ZO-1↑, enhance the integrity of the intestinal epithelial barrier by upregulating the expression of tight junction proteins such as occludin and zonula occludens-1 (ZO-1) [51,54].
AntiTum↑, Certain polysaccharides in Aloe Vera, including acemannan, have demonstrated antitumoral effects by inducing apoptosis (programmed cell death) in cancer cells.
Casp3↑, This is achieved through the activation of caspase-3 and caspase-9, key enzymes in the apoptotic pathway [45,48].
Casp9↑,
angioG↓, Aloe Vera polysaccharides also inhibit angiogenesis and metastasis by downregulating matrix metalloproteinases (MMPs) and VEGF [75].
MMPs↓,
VEGF↓,
NK cell↑, Moreover, these polysaccharides enhance the immune system’s ability to recognize and destroy cancer cells through stimulating natural killer (NK) cells and cytotoxic T lymphocytes (CTLs) [43,55].
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Melanoma, |
B16-F10 |
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other↓, Baicalein significantly inhibited melanin synthesis in a concentration-dependent manner without cytotoxicity
other?, Tyrosinase activity was also reduced.
ERK↑, Western blotting showed that baicalein induced ERK activation
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Var, |
NA |
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IBD, |
NA |
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Inflam↓, anti-inflammatory, antidiabetic, antibacterial, antiparasitic, antidiarrheal, antihypertensive, hypolipidemic, and fungicide.
AntiCan↑, elaborated on the anticancer effects of BBR through the regulation of different molecular pathways such as: inducing apoptosis, autophagy, arresting cell cycle, and inhibiting metastasis and invasion.
Apoptosis↑,
TumAuto↑,
TumCCA↑,
TumMeta↓,
TumCI↓,
eff↑, BBR is shown to have beneficial effects on cancer immunotherapy.
eff↑, BBR inhibited the release of Interleukin 1 beta (IL-1β), Interferon gamma (IFN-γ), Interleukin 6 (IL-6), and Tumor Necrosis Factor-alpha (TNF-α) from LPS stimulated lymphocytes by acting as a dopamine receptor antagonist
CD4+↓, BBR inhibited the proliferation of CD4+ T cells and down-regulated TNF-α and IL-1 and thus, improved autoimmune neuropathy.
TNF-α↓,
IL1↓,
BioAv↓, On the other hand, P-Glycoprotein (P-gp), a secretive pump located in the epithelial cell membrane, restricts the oral bioavailability of a variety of medications, such as BBR. The use of P-gp inhibitors is a common and effective way to prevent this
BioAv↓, Regardless of its low bioavailability, BBR has shown great therapeutic efficacy in the treatment of a number of diseases.
other↓, BBR has been also used as an effective therapeutic agent for Inflammatory Bowel Disease (IBD) for several years
AMPK↑, inhibitory effects on inflammation by regulating different mechanisms such as 5′ Adenosine Monophosphate-Activated Protein Kinase (AMPK. Increase of AMPK
MAPK↓, Mitogen-Activated Protein Kinase (MAPK), and NF-κB signaling pathways
NF-kB↓,
IL6↓, inhibiting the expression of proinflammatory genes such as IL-1, IL-6, Monocyte Chemoattractant Protein 1 (MCP1), TNF-α, Prostaglandin E2 (PGE2), and Cyclooxygenase-2 (COX-2)
MCP1↓,
PGE2↓,
COX2↓,
*ROS↓, BBR protected PC-12 cells (normal) from oxidative damage by suppressing ROS through PI3K/AKT/mTOR signaling pathways
*antiOx↑, BBR therapy improved the antioxidant function of mice intestinal tissue by enhancing the levels of glutathione peroxidase and catalase enzymes.
*GPx↑,
*Catalase↑,
AntiTum↑, Besides, BBR leaves great antitumor effects on multiple types of cancer such as breast cancer,69 bladder cancer,70 hepatocarcinoma,71 and colon cancer.72
TumCP↓, BBR exerts its antitumor activity by inhibiting proliferation, inducing apoptosis and autophagy, and suppressing angiogenesis and metastasis
angioG↓,
Fas↑, by increasing the amounts of Fas receptor (death receptor)/FasL (Fas ligand), ROS, ATM, p53, Retinoblastoma protein (Rb), caspase-9,8,3, TNF-α, Bcl2-associated X protein (Bax), BID
FasL↑,
ROS↑,
ATM↑,
P53↑,
RB1↑,
Casp9↑,
Casp8↑,
Casp3↓,
BAX↑,
Bcl-2↓, and declining Bcl2, Bcl-X, c-IAP1 (inhibitor of apoptosis protein), X-linked inhibitor of apoptosis protein (XIAP), and Survivin levels
Bcl-xL↓,
IAP1↓,
XIAP↓,
survivin↓,
MMP2↓, Furthermore, BBR suppressed Matrix Metalloproteinase-2 (MMP-2), and MMP-9 expression.
MMP9↓,
CycB/CCNB1↓, Inhibition of cyclin B1, cdc2, cdc25c
CDC25↓,
CDC25↓,
Cyt‑c↑, BBR inhibited tumor cell proliferation and migration and induced mitochondria-mediated apoptosis pathway in Triple Negative Breast Cancer (TNBC) by: stimulating cytochrome c release from mitochondria to cytosol
MMP↓, decreased the mitochondrial membrane potential, and enabled cytochrome c release from mitochondria to cytosol
RenoP↑, BBR significantly reduced the destructive effects of cisplatin on the kidney by inhibiting autophagy, and exerted nephroprotective effects.
mTOR↓, U87 cell, Inhibition of m-TOR signaling
MDM2↓, Downregulation of MDM2
LC3II↑, Increase of LC3-II and beclin-1
ERK↓, BBR stimulated AMPK signaling, resulting in reduced extracellular signal–regulated kinase (ERK) activity and COX-2 expression in B16F-10 lung melanoma cells
COX2↓,
MMP3↓, reducing MMP-3 in SGC7901 GC and AGS cells
TGF-β↓, BBR suppressed the invasion and migration of prostate cancer PC-3 cells by inhibiting TGF-β-related signaling molecules which induced Epithelial-Mesenchymal Transition (EMT) such as Bone morphogenetic protein 7 (BMP7),
EMT↑,
ROCK1↓, inhibiting metastasis-associated proteins such as ROCK1, FAK, Ras Homolog Family Member A (RhoA), NF-κB and u-PA, leading to in vitro inhibition of MMP-1 and MMP-13.
FAK↓,
RAS↓,
Rho↓,
NF-kB↓,
uPA↓,
MMP1↓,
MMP13↓,
ChemoSen↑, recent studies have indicated that it can be used in combination with chemotherapy agents
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NSCLC, |
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PC, |
NA |
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HCC, |
NA |
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Dose↝, Huachansu was administered intravenously for 14 days followed by 7 days off (1 cycle). 10 (level 1), 20 (level 2), 40 (level 3), 60 (level 4), and 90 (level 5) mL/m2.
toxicity↓, Mild adverse events were observed at each dose level; all were grade I or II and no grade III or IV toxicities were observed.
other↓, One of these patients (with hepatocellular cancer) had 20% regression (duration = 11 months) (dose level 1).
QoL↑, Quality of life improved for patients with stable disease.
OS?, Six patients had prolonged stable disease or minor tumor shrinkage.
*Inflam↓, anticancer, anti-edema, anti-inflammatory, anti-microbial, anti-coagulant, anti-osteoarthritis, anti-trauma pain, anti-diarrhea, wound repair.
*Bacteria↓,
*Pain↓,
*Diar↓,
*Wound Healing↑,
ERK↓, Figure 1
JNK↓,
XIAP↓,
HSP27↓,
β-catenin/ZEB1↓,
HO-1↓,
lipid-P↓,
ACSL4↑,
ROS↑,
SOD↑,
Catalase↓,
GSH↓,
MDA↓,
Casp3↓,
Casp9↑,
DNAdam↑,
Apoptosis↑,
NF-kB↓,
P53↑,
MAPK↓,
APAF1↑,
Cyt‑c↓,
CD44↓,
Imm↑, Bromelain was also studied in the innate immune system, where it could enhance and sustain the process
ATG5↑,
LC3I↑,
Beclin-1↑,
IL2↓, bromelain in vitro experiments resulted in diminished amounts of IL-2, IL-6, IL-4, G-CSF, Gm-CSF, IFN-γ,
IL4↓,
IFN-γ↓,
COX2↓, proprietary bromelain extract could decrease IL-8, COX-2, iNOS, and TNF-α without affecting cell viability.
iNOS↓,
ChemoSen↑, Bromelain may increase the cytotoxicity of cisplatin in the treatment of breast cancer as reported in 2 studies with MDA-MB-231 and 4T1 Breast Tumor cell lines
RadioS↑, The size and weight of tumors in gamma-irradiated EST-bearing mice treated with bromelain decreased significantly with a significant amelioration in the histopathological examination
Dose↝, oral bromelain administration in breast cancer patients (daily up to a dose of 7800 mg)
other↓, The role of bromelain (in combination with papain, sodium selenite and Lens culinaris lectin) has been also tested as a complementary medicine on more than 600 breast cancer patients to reduce the side effects caused by the administration of the adju
other↓, prostatic volumes in men whose prostates were biopsied (p < 0.012) was significantly lower in the study group as compared with those in the control group 2
other↓, BA and BX are safe and non-genotoxic under the in vitro conditions and can alleviate cytotoxic, oxidative, and genetic damage induced by 3-MCPD in the human blood cells.
HCAR2↑, Millimolar concentrations of butyrate are needed to activate the receptor.
other↓, The expression of GPR109A is silenced in colon cancer in humans, in a mouse model of intestinal/colon cancer, and in colon cancer cell lines.
Apoptosis↑, Re-expression of GPR109A in colon cancer cells induces apoptosis, but only in the presence of its ligands butyrate and nicotinate.
HDAC↓, Butyrate is an inhibitor of histone deacetylases, but apoptosis induced by activation of GPR109A with its ligands in colon cancer cells does not involve inhibition of histone deacetylation.
Bcl-2↓, primary changes in this apoptotic process include downregulation of Bcl-2, Bcl-xL, and cyclin D1, and upregulation of death receptor pathway.
Bcl-xL↓,
cycD1/CCND1↓,
DR5↑,
NF-kB↓, In addition, GPR109A/butyrate suppresses NF-κB activation in normal and cancer colon cell lines as well as in normal mouse colon.
GutMicro↑, Gut bacteria play a critical role in the prevention of colon cancer and inflammatory bowel disease
SLC12A5↝, We have shown previously that butyrate induces apoptosis in colon cancer cell lines if SLC5A8, a butyrate transporter, is expressed in these cells and that the process is associated with inhibition of HDACs
chemoPv↑, capsaicin has been reported as both a chemopreventive and as an anticancer agent
AntiCan↑,
ROS↑, Capsaicin has been reported to induce ROS-dependent cell death in various cancers, including colorectal [63], prostate [64,65], bladder [66,67,68], and pancreatic [69,70] cancers.
TumCG↓, reported to inhibit tumor growth in vivo in mouse xenograft models of prostate [64] and bladder [66] cancers.
ROS↑, Mechanistically, capsaicin-mediated ROS accumulation
MMP↑, leads to mitochondrial membrane depolarization [63,64,66],
Apoptosis↑, which further triggers mitochondria-dependent apoptosis
TumCCA↑, as well as G0/G1 cell cycle arrest
JNK↑, in bladder cancer cells, capsaicin induces JNK activation in an ROS-dependent manner
SOD↓, (1) inhibition of the activity of antioxidant enzymes SOD, catalase (CAT), and glutathione peroxidase [70];
Catalase↓,
GPx↓,
other↓, (2) inhibition of the activity of mitochondrial complex-I and complex-III in the electron transport chain [70];
SIRT1↓, (3) downregulation of the expression of sirtuin-1, a NAD-dependent deacetylase that regulates the expression of various antioxidant enzymes [69];
NADPH↑, (4) upregulation of the expression of NADPH oxidase 4, which generates superoxide [69];
FOXO3↑, (5) increased expression of FOXO3a, which is a transcription factor that regulates the oxidative stress response [68].
*other↓, When OS-induced TRPM2 and GSK-induced TRPV4 activations were inhibited by the treatment of CARV
*GSH↑, upregulation of glutathione and glutathione peroxidase.
*GPx↑,
*ROS↓, The possible TRPM2 and TRPV4 blocker action of carvacrol (CARV) via the modulation oxidative stress and apoptosis in the SH-SY5Y neuronal cells.
*Apoptosis↓,
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Park, |
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*memory↑, Carvacrol enhances memory and cognition by modulating the effects of oxidative stress, inflammation, and Aβ25-35-induced neurotoxicity in AD
*cognitive↑,
*ROS↓, reduces the production of reactive oxygen species and proinflammatory cytokine levels in PD
*Inflam↓,
*motorD↑, improves motor functions
*toxicity↓, in general, it is potentially safe for consumption
*TRPV3↑, Carvacrol is a potent agonist of transient receptor potential vanilloid 3 (TRPV3)
*other↓, mitigating oxidative stress (OS)/ADP-ribose (ADPR)-induced TRPM2 and GSK1016790A (GSK)-mediated TRPV4 activations
*antiOx↑, Essential oils, high in carvacrol, have powerful antioxidant properties [85-88] similar to vitamin E, ascorbic acid, and butyl hydroxyl toluene
*LDL↓, Low-density lipoprotein (LDL) is inhibited by carvacrol in vitro and mediates LDL oxidation within an incubation period of 12 h
*COX2↓, suppressing the expression level of cyclooxygenase-2 (COX-2),
*PPARα↑, triggering the peroxisome proliferator-activated receptors (PPAR) α and γ
*NO↓, inhibiting NO production
*AChE↓, Carvacrol's acetylcholinesterase inhibitory action is 10 times higher than thymol's, even though the two compounds have a relatively similar structure
*eff↑, carvacrol nanoemulsion treatment has shown more notable effects compared to carvacrol oil.
*SOD↑, increases superoxide dismutase (SOD) and catalase (CAT) activity
*Catalase↑,
*neuroP↑, neuroprotective effects of carvacrol against cognitive impairments and its potential in AD are shown in Fig. (2)
*BioAv↝, In rabbits, 1.5 g of orally administered carvacrol is progressively absorbed from the intestines, with approximately 30% of the whole dose remaining in the gastrointestinal system and 25% eliminated via urine after 22 h of administratio
*BBB↑, carvacrol in the brain tissues as it easily crosses the blood-brain barrier owing to its low molecular weight (150.2 g/mol) and higher lipophilicity
*BioAv↑, liposomal encapsulation [136], and solid lipid nanoparticles [137], were developed and found bioavailable on oral administration. These formulations exhibit improved solubility, stability, and bioavailability and enhance drug accumulation in the tiss
chemoPv↑, It has been widely studied as chemopreventive and anticancer drug
Catalase↑,
ROS↑, ROS induction has been attributed as the primary mode through which celastrol mediates its anticancer effects.
HSP90↓, celastrol has been reported to inhibit HSP90 function
Sp1/3/4↓, induce suppressor of specificity protein (Sp) repressors [79], activate the PKCzeta–AMPK-p53–PLK 2 signaling axis [73], and activate the JNK pathway [80,81] to induce apoptosis.
AMPK↑,
P53↑,
JNK↑,
ER Stress↑, celastrol induces ER stress [78], mitochondrial dysfunction, specifically disruption of mitochondrial membrane potential [72,78,82], and cell cycle arrest at G2/M phase [76,77] and S phase [75]
MMP↓,
TumCCA↑,
TumAuto↑, Interestingly, at low concentrations (i.e., below the cytotoxic threshold) celastrol was found to induce autophagy in gastric cancer cells through ROS-mediated accumulation of hypoxia-inducible factor 1-α via the transient activation of AKT.
Hif1a↑,
Akt↑,
other↓, (1) inhibition of mitochondrial respiratory chain complex I activity [80];
Prx↓, (2) inhibition of peroxiredoxins, namely peroxiredoxin-1 [76] and peroxiredoxin-2 [78].
*toxicity↓, which indicated no significant evidence of toxic or adverse effects following acute oral exposure
*antiOx↑, CQAs have antioxidant [68], antibacterial [69], antiviral [70], antidiabetic [71], neuroprotective [72,73], anti-inflammatory [74], and cytostatic effects [75,76].
*Bacteria↓,
*AntiDiabetic↑,
*neuroP↑, Several in vivo studies have demonstrated the neuroprotective properties of 5-CQA
*Inflam↓,
*cardioP↑, CQAs have been used therapeutically in some clinical treatments as well, e.g., in the treatment of cardiovascular diseases [77] and arterial hypertension (high blood pressure)
*BP↓,
*other↓, CQA (i.g.) in doses of 50–200 mg/kg bw (aluminum chloride (AlCl3), 35 mg/kg bw per day) weakens aluminum-induced Al3+-accumulation, oxidative stress, mitochondrial damage, and nuclear pyknosis in the hippocampus
eff↓, Chlorogenic acid has been found to counteract the effects of metformin, a pharmaceutical drug used to manage elevated blood sugar levels. only observed at high levels of chlorogenic acid, which is unlikely to occur in humans
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AD, |
NA |
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Stroke, |
NA |
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*eff↑, CA and NCA increased the recovery of synaptic transmission upon re-oxygenation following 7 min of oxygen/glucose deprivation, an in vitro ischemia model.
*other↓, CA and NCA attenuated the shift of LTD into LTP observed in hippocampal slices from animals with hippocampal-dependent memory deterioration after exposure to β-amyloid 1–42 (2 nmol, icv), in the context of Alzheimer’s disease.
*Risk↓, The regular consumption of moderate amounts of coffee affords a robust protection against age-associated chronic diseases
*cognitive↑, Brain diseases are a major burden of disease5 and coffee intake dampens neuropsychiatric diseases with a robust inverse relation between coffee intake and mood-related depressive conditions6–8 as well as with cognitive deterioration
*neuroP↑, Caffeine is a major constituent of coffee involved in these neuroprotective effects
*antiOx↑, As most polyphenols, chlorogenic acids have been described as potent antioxidants
other↓, During chemotherapy, homocysteine (P = 0.032) and vitamin B12 (P < 0.001) concentrations increased, while folate and platelets decreased (decreases with supplements)
other↝, we also verified a correlation between Hcy levels and cofactors (B12 vitamin and folate).
homoC↓, The anti‐DNA action of alkylating agents would lead to a reduction of folic acid and vitamin B12 concentrations, which in turn would lead to an increase of homocysteine concentration (supplements would lower homoC)
eff↝, As seen in this study, vitamin B12 and folic acid concentrations decreased with the progression of treatment, and they are inversely related to homocysteine levels.
other↝, increase homocysteine concentration 6 months after chemotherapy, as well as a significant decrease in vitamin B12, folic acid, and platelets at the third and sixth month after beginning of chemotherapy treatment in women with BC.
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Nor, |
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NA |
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*lipid-P↓, inhibition of lipid peroxidation and the protection of LDL-cholesterol against oxidation, and increase resistance to oxidative stress.
*ROS↓,
*Inflam↓, decreasing platelet function and inflammation along with diastolic and systolic arterial pressures, which, taken together, may reduce the risk of cardiovascular mortality.
*BP↓,
*cardioP↑, Epidemiological studies demonstrate that regular dietary intake of cocoa polyphenols reduces the risk of coronary heart disease and stroke and is inversely associated with the risk of cardiovascular disease.
*chemoPv↑, They also have antiproliferative, antimutagenic, and chemoprotective effects, in addition to their anticariogenic effects.
*BioAv⇅, great controversy surrounding the bioavailability of phenolics in general and of cocoa derivatives in particular.
*antiOx↑, Cocoa has more phenolics and higher antioxidant capacity than green tea, black tea, or red wine
*Risk↓, Epidemiological studies demonstrate that regular dietary intake of cocoa polyphenols reduces the risk of coronary heart disease and stroke and is inversely associated with the risk of cardiovascular disease.
*5LO↓, cocoa polyphenols decrease the plasma concentration of proinflammatory cysteinyl leukotrienes through inhibition of 5-LOX, as demonstrated by Sies et al.
*AntiAg↑, Moreover, cocoa decreases not only platelet aggregation, but also adhesion. 234 mg cocoa phenolics a day for 28 days
*Imm↑, Kenny et al. [21] demonstrated that cocoa oligomers are potent stimulators of both the innate immune system and early events in adaptive immunity.
*NF-kB↓, nd their dimeric forms were found to inhibit the NF-κB activation induced by 12-O-tetradecanoylphorbol-13-acetate (TPA) in T cells,
*other↓, in vivo and in vitro models have provided evidence that pure polyphenols and natural polyphenol plant extracts can modulate intestinal inflammation.
CYP1A1↓, polyphenol cocoa extract leads to the induction of CYP1A1 in breast cancer cells.
COX2↓, hey also inhibited the expression of COX-2,
*Obesity↓, Ferrazzano et al. hypothesized that the polyphenols contained in cocoa may have antiobesity effects due to their ability to suppress fatty acid synthesis while stimulating cell energy expenditure in the mitochondria
*cognitive↑, Moreover, cocoa consumption may also have beneficial effects on satiety, cognitive function, and mood [93].
ACLY↓, administration of citrate at high level mimics a strong inhibition of ACLY and could be tested to strengthen the effects of current therapies.
-a strong ACLY inhibition could be mimicked by by flooding the cytosol with citrate.
other↓, ACLY inhibition by simple drugs such as HCA or bempedoic acid should be tested, optimally
associated with glycolytic inhibitors (or glucose starvation diet) and current therapies.
PFK1↓, citrate promotes: - the inactivation of PFK1 and decreases ATP production [
ATP↓,
PFK2↓, inhibition of PFK2 in ascite cancer cells
Mcl-1↓, deactivation of the anti-apoptotic factor Mcl-1 and the activation of caspases such as
caspase 2, 3 and 9
Casp3↑,
Casp2↑,
Casp9↑,
IGF-1R↓, downregulation of the IGF-1R/PI3K/AKT
PI3K↓,
Akt↓,
p‑Akt↓, decreased phosphorylation of AKT and ERK in non-small cell lung cancer
p‑ERK↓,
PTEN↑, activation of PTEN suppressor,
Snail↓, reversion of dedifferentiation (in particular through Snail inhibition with E-cadherin expression) and stimulation of T lymphocytes response
E-cadherin↑,
ChemoSen↑, increasing the sensitivity of tumors to cisplatin
*other↓, Our finding suggests that CoQ10 inhibits the activation of PSCs by suppressing autophagy through activating the PI3K/AKT/mTOR signaling pathway.
*PI3K↑, PI3K/AKT/mTOR signaling pathway were dose-dependently upregulated with increased CoQ10 concentrations
*Akt↑,
*mTOR↑,
*ROS↓, In this study, CoQ10 significantly reduced the intracellular level of ROS in PSCs.
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Stroke, |
NA |
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*other↑, anti-Alzheimer properties of saffron extract were shown in human and animal studies.
*monoA↑, increased glutamate and dopamine levels in the brain in a dose-dependent manner.
*Aβ↓, C. sativus stigmas has good antioxidant properties -higher than those of carrot and tomato- in a concentration and time-dependent manner which was accompanied by inhibition of Aβ fibrillogenesis.
*AChE↓, saffron extract had a moderate (up to 30 %) inhibitory activity on acetyl-cholinesterase (AChE)
*cognitive↑, results showed that the cognitive functions in saffron-treated group were significantly better than placebo
*neuroP↑, Neuroprotective effects of seven-day administration of crocetin
*lipid-P↓, crocin 10 μM inhibited the formation of peroxidized lipids in cultured PC12 cells, moderately restored superoxide dismutase (SOD) activity
*SOD↑,
*ROS↓, protective effects on different markers of oxidative damage in hippocampal tissue from ischemic rats
*GPx↑, crocin increased the activity of SOD and glutathione peroxidase (GPx) and remarkably reduced malondialdehyde (MDA) content in the ischemic cortex in rat model of ischemic stroke
*MDA↓,
*memory↑, Saffron extract and crocin can improve learning and memory
*antiOx↑, crocetin increases the antioxidant potential in brain and helps to fight against 6-OHDA-induced neurotoxicity
*Inflam↓, prevented diazinon (20 mg/kg)-induced increase of inflammation
*other↓, Administration of crocin (60 mg/kg), one hour before, or one hour after the induction of ischemia, reduced brain edema
*ER Stress↓, Administration of crocin on day 7 post-EAE induction, suppressed ER stress and inflammatory gene expression in the spinal cord
*AChE↓, Previously we have reported curcumin to induce mortality in Cx. pipiens by inhibiting AChE.
*other↓, The next hit, gingerol, is also reported to be an AChE inhibitor [61].
*other↓, Capsaicin, a phytochemical is reported to be AChE inhibitor [62].
*other↓, Rosmarinic acid is a polyphenol found in multiple aromatic plants and is reported to inhibit glutathione S-transferase, lactoperoxidase, AChE, BChE and carbonic anhydrase isoenzymes
*other↓, The next hit, piperine is known to inhibit ChEs, moreover curcumin and piperine are reported to synergically inhibit AChE and BChE in humans
*other↓, Sesamin is a phytochemical found in Cortex Acanthopanacis radicis, is reported to inhibit AChE, and known to improve memory impairment in mouse [65]
*other↓, Lastly as represented earlier, ursolic and oleanolic acid from the leaves of C. talcana are reported to inhibit AChE [14]
*AntiCan↑, EGCG’s therapeutic potential in preventing and managing a range of chronic conditions, including cancer, cardiovascular diseases, neurodegenerative disorders, and metabolic syndromes
*cardioP↑,
*neuroP↑,
*BioAv↝, Factors such as fasting, storage conditions, albumin levels, vitamin C, fish oil, and piperine have been shown to affect plasma concentrations and the overall bioavailability of EGCG
*BioAv↓, Conversely, bioavailability is reduced by processes such as air oxidation, sulfation, glucuronidation, gastrointestinal degradation, and interactions with Ca2+, Mg2+, and trace metals,
*BioAv↓, EGCG’s oral bioavailability is generally low, with marked differences observed across species, for example, bioavailability rates of 26.5% in CF-1 mice and just 1.6% in Sprague Dawley rats
*Dose↝, plasma concentrations exceeded 1 μM only when doses of 1 g or higher were administered.
*Half-Life↝, Specifically, a dose of 1600 mg yielded a Cmax of 3392 ng/mL (range: 130–3392 ng/mL), with peak levels observed between 1.3 and 2.2 h, AUC (0–∞) values ranging from 442 to 10,368 ng·h/mL, and a half-life (t1/2z) of 1.9 to 4.6 h.
*BioAv↑, Studies on the distribution of EGCG have revealed that, despite its limited absorption, it is rapidly disseminated throughout the body or quickly converted into metabolites
*BBB↑, Additionally, EGCG can cross the blood–brain barrier, allowing it to reach the brain
*hepatoP↓, Several studies have documented liver damage linked to green tea consumption [48,49,50,51,52,53].
*other↓, EGCG has also been shown to inhibit the intestinal absorption of non-heme iron in a dose-dependent manner in a controlled clinical trial
*Inflam↓, EGCG has been widely recognized for its anti-inflammatory effects
*NF-kB↓, EGCG has been shown to suppress NF-κB activation, inhibit its nuclear translocation, and block AP-1 activity
*AP-1↓,
*iNOS↓, downregulation of pro-inflammatory enzymes like iNOS and COX-2 and scavenging of ROS/RNS, including nitric oxide and peroxynitrite
*COX2↓,
*ROS↓,
*RNS↓,
*IL8↓, EGCG has been shown to suppress airway inflammation by reducing IL-8 release, a cytokine involved in neutrophil aggregation and ROS production.
*JAK↓, EGCG blocks the JAK1/2 signaling pathway
*PDGFR-BB↓, downregulate PDGFR and IGF-1R gene expression
*IGF-1R↓,
*MMP2↓, reduce MMP-2 mRNA expression
*P53↓, downregulation of the p53-p21 signaling pathway and the enhanced expression of Nrf2
*NRF2↑,
*TNF-α↓, 25 to 100 μM reduced the levels of TNF-α, IL-6, and ROS while enhancing the expression of E2F2 and superoxide dismutases (SOD1 and SOD2), enzymes vital for cellular antioxidant defense.
*IL6↓,
*E2Fs↑,
*SOD1↑,
*SOD2↑,
Casp3↑, EGCG has been shown to activate key apoptotic pathways, such as caspase-3 activation, cytochrome c release, and PARP cleavage, in various cell models, including PC12 cells exposed to oxidative stress
Cyt‑c↑,
PARP↑,
DNMTs↓, (1) the inhibition of DNA hypermethylation by blocking DNA methyltransferase (DNMT)
Telomerase↓, (2) the repression of telomerase activity;
Hif1a↓, (3) the suppression of angiogenesis via the inhibition of HIF-1α and NF-κB;
MMPs↓, (4) the prevention of cellular metastasis by inhibiting matrix metalloproteinases (MMPs);
BAX↑, (5) the promotion of apoptosis through the activation of pro-apoptotic proteins like BAX and BAK
Bak↑,
Bcl-2↓, while downregulating anti-apoptotic proteins like BCL-2 and BCL-XL;
Bcl-xL↓,
P53↑, (6) the upregulation of tumor suppressor genes such as p53 and PTEN;
PTEN↑,
TumCP↓, (7) the inhibition of inflammation and proliferation via NF-κB suppression;
MAPK↓, (8) anti-proliferative activity through the modulation of MAPK and IGF1R pathways
HGF/c-Met↓, EGCG inhibits hepatocyte growth factor (HGF), which is involved in tumor migration and invasion
TIMP1↑, EGCG has also been shown to influence the expression of tissue inhibitors of metalloproteinases (TIMPs) and MMPs, which are involved in tumorigenesis
HDAC↓, nhibition of UVB-induced DNA hypomethylation and modulation of DNMT and histone deacetylase (HDAC) activities
MMP9↓, inhibiting MMPs such as MMP-2 and MMP-9
uPA↓, EGCG may block urokinase-like plasminogen activator (uPA), a protease involved in cancer progression
GlutMet↓, EGCG can exert antitumor effects by inhibiting glycolytic enzymes, reducing glucose metabolism, and further suppressing cancer-cell growth
ChemoSen↑, EGCG’s combination with standard chemotherapy drugs may enhance their efficacy through additive or synergistic effects, while also mitigating chemotherapy-related side effects
chemoP↑,
other↝, the peak powers of the high-voltage pulsed power supplies with load resistances in the range of
1–50 U were all greater than 1 MW, and the energies were all greater than 0.03 J.
other↝, currently, the maximum output frequency is 50 Hz due to restrictions in mechanical rotational
energy.
Ca+2↑, This indicated a rapid increase in intracellular Ca 2+ , as the electrical pulse triggered the
release of Ca2+ from the endoplasmic reticulum.
TumCD↑, Nanosecond pulse stimulation induces tumor ablation
and immunity activation
Imm↑,
TumCG↓, Nanosecond pulses inhibit distal tumor growth
other↓, With a material cost of only around $15, it is a fraction of the price of commercial
NPGs, which typically cost tens of thousands of dollars.
*BDNF↑, a healthy lifestyle, exercise, and dietary modifications are shown to positively influence insulin regulation in the brain, reduce inflammation, and up-regulate the levels of BDNF, and are thus expected to have roles in AD
*eff↑, Donepezil and galantamine (Acetylcholinesterase inhibitor) treated animal and human patients have shown to have higher levels of BDNF
*other↓, decline in BDNF levels is linked to increasing age, and it is more noticeable in females, the elderly, and those with higher body weights (Komulainen et al., 2008; Lee et al., 2009). The decline correlates with memory loss and hippocampal atrophy
*eff↑, A single aerobic exercise session done consistently was associated with a higher increase in BDNF levels compared to if done acutely
*other↓, Significant reductions in GABA levels have been described in severe cases of AD, which could be underlying the behavioral and psychological symptoms of AD.
other↓, no-observed-adverse-effect-level (NOAEL) was determined to be 2000 mg/kg bw/day.
other↓, anti-tumor, antiviral, antibacterial, antioxidant, immune regulation, production of hypoglycemic lipids, scavenging free radicals, and stimulating the hematopoietic system
lactateProd↓, LDHA inhibitor gossypol
other↓, Remarkably, we found no fibrosis at any level in any mice that were irradiated and received gossypol (Fig. 1D). Together, these results indicate that gossypol inhibited radiation-induced pulmonary fibrosis.
TGF-β↓, Gossypol Inhibits Radiation-Induced TGF-β
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NA, |
NA |
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Nor, |
NA |
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other↓, water leaves extract of A. muricata had no anticancer effect at all
*toxicity↓, no cytotoxic effect on normal spleen cells
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*antiOx↑, antioxidative properties as it directly neutralizes hydroxyl radicals and reduces peroxynitrite level
*NRF2↑, activates Nrf2 and HO-1, which regulate many antioxidant enzymes and proteasomes.
*HO-1↑,
*Inflam↓, hydrogen may prevent inflammation
*neuroP↑, prevention and treatment of various ageing-related diseases, such as neurodegenerative disorders, cardiovascular disease, pulmonary disease, diabetes, and cancer.
*cardioP↑,
*other↓, It also prevented ischemia-reperfusion (I/R) injury and stroke in a rat model
*ROS↓, H2 has been shown to exert its beneficial effects in various pathological conditions that involve free radicals and oxidative stress
*NADPH↓, figure 2, H2 Inhibits NADPH Oxidase Activity
*Catalase↑,
*GPx1↑,
*NO↓, H2 Indirectly Reduces Nitric Oxide (NO) Production
*mt-ROS↓, H2 Decreases Mitochondrial ROS
*SIRT3↑, In the kidneys, H2 suppressed the downregulated Sirt3 expression, which is the most abundant member of the sirtuin family, by reducing oxidative stress reactions
*SIRT1↑, In the liver, H2 elevated HO-1 to induce Sirt1 expression
*TLR4↓, H2 inhibits TLR4, which involves hyperglycemia in type 2 diabetes mellitus
*mTOR↓, For example, H2 inhibits mTOR, activates autophagy, and alleviates cognitive impairment resulting from sepsis
*cognitive↑,
*Sepsis↓,
*PTEN↓, It inhibits the activation of the PTEN/AKT/mTOR pathway and alleviates peritoneal fibrosis
*Akt↓,
*NLRP3↓, It also facilitates autophagy-mediated NLRP3 inflammasome inactivation and alleviates mitochondrial dysfunction and organ damage
*AntiAg↑, antiageing mechanism of H2 and the influence on ageing hallmarks are summarized in Figure 3.
*IL6↓, significantly suppressed inflammatory cytokines (IL-6, TNF-α, and IL-1β), MDA, and 8-OHdG, and improved memory dysfunction
*TNF-α↓,
*IL1β↓,
*MDA↓,
*memory↑,
*FOXO3↑, HRW can also upregulate Sirt1-Forkhead box protein O3a (FOXO3a
TumCG↓, H2 inhibits lung cancer progression
*LDL↓, Decreases oxidized LDL; improves HDL function
*other↓, HCA administration significantly reduced crystal deposition and kidney injury induced by glyoxylate
*ROS↓, alleviated oxidative stress via upregulating the antioxidant enzyme activities of superoxide dismutase (SOD) and catalase (CAT) and reducing the malondialdehyde (MDA) content
*SOD↑,
*Catalase↑,
*MDA↓,
*NRF2↑, via activating Nrf2/Keap1
ChemoSen↑, short-term fasting or autophagy-inducing caloric restriction mimetics, such as hydroxycitrate and spermidine, improves the antitumor efficacy of chemotherapy in vivo
eff↑, combination of MTX and HC (but neither of these two agents alone) markedly reduced the frequency of tumor-infiltrating CD4+CD25+Foxp3+ Tregs
ACLY↓, HC acts as a competitive inhibitor of the ATP citrate lyase (ACLY)
LC3‑Ⅱ/LC3‑Ⅰ↑, ACLY inhibitors (SB-204990, BMS-303141) stimulated autophagic flux in cultured cancer cells, as indicated by the autophagy-associated conversion of LC3 I to LC3 II
TumAuto↑, starvation can enhance chemotherapy-induced immunosurveillance in an autophagy-dependent fashion.
other↓, causes Treg depletion, which in turn improves immunosurveillance against KRas-induced neoplasia.
ACLY↓, Hydroxycitrate is a known inhibitor of ATP citrate lyase ( also called ATP-citric synthase
other↓, Lipoic Acid Increases PDC (pyruvate dehydrogenase complex)
ROS↑, oxidative onslaught, making the cancer cell susceptible to oxidative therapies such as alpha lipoic acid.
eff↑, the addition of hydroxycitrate increases the effect of ALA.
PDKs↓, An inhibitory effect of lipoic acid on PDKs would result in… increased PDC pyruvate dehydrogenase complex (PDC) activity.
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Nor, |
HUVECs |
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*other↓, HCA effectively attenuated lung injury, inflammation, and edema induced by ischemia reperfusion
*Inflam↓,
*MDA↓, HCA treatment significantly reduced malondialdehyde (MDA) and reactive oxygen species (ROS) levels
*ROS↓,
*Iron↓, while decreasing iron content and increasing superoxide dismutase (SOD)
*SOD↓,
*Hif1a↓, HCA administration significantly inhibited Hif-1α and HO-1 upregulation both in vivo and in vitro.
*HO-1↓,
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Melanoma, |
NA |
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CRC, |
HCT116 |
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TumAuto↓, Inhibition of autophagy by administration of chloroquine (CQ) in combination anticancer therapies is currently evaluated in clinical trials.
eff↓, targeting autophagy in the tumor environment by CQ may be limited to well-perfused regions but not achieved in acidic regions, predicting possible limitations in efficacy of CQ in antitumor therapies.
other↓, CQ concentrations in the whole-cell lysate were 7-fold lower at pH 6.8 as compared with pH 7.4
other↓, Quinones are among the rare compounds successfully used as therapeutic agents to correct mitochondrial diseases and as specific regulators of mitochondrial function within cells.
ROS↑, The stimulation of ROS production by juglone and 2,5-di-tert-butyl-1,4-benzoquinone
MMP↓, dissipation of the mitochondrial membrane potential
eff↝, all the quinones, except for coenzyme Q10, decreased the mitochondrial membrane potential. Juglone, 1,4-benzoquinone, and menadione showed the most pronounced effects.
Showing Research Papers: 1 to 50 of 100
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 100
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
Catalase↓, 2, Catalase↑, 1, CYP1A1↓, 1, Ferroptosis↑, 1, GPx↓, 1, GSH↓, 2, GSH↝, 1, HO-1↓, 1, Iron↑, 1, lipid-P↓, 1, MDA↓, 1, Mets↑, 1, OXPHOS↓, 1, Prx↓, 1, ROS↑, 10, mt-ROS↑, 1, SOD↓, 1, SOD↑, 1,
Mitochondria & Bioenergetics ⓘ
ATP↓, 1, ATP∅, 1, CDC25↓, 2, compIII↑, 1, mitResp↓, 1, MMP↓, 3, MMP↑, 1, XIAP↓, 2,
Core Metabolism/Glycolysis ⓘ
ACLY↓, 3, ACSL4↑, 1, AMPK↑, 4, FDG↓, 1, GlucoseCon↓, 1, GlutMet↓, 1, homoC↓, 1, lactateProd↓, 1, NADPH↑, 1, PDH↑, 1, PDKs↓, 1, PFK1↓, 1, PFK2↓, 1, SIRT1↓, 1,
Cell Death ⓘ
Akt↓, 1, Akt↑, 1, p‑Akt↓, 1, APAF1↑, 1, Apoptosis↑, 6, Bak↑, 2, BAX↑, 3, Bcl-2↓, 3, Bcl-xL↓, 3, Casp2↑, 1, Casp3↓, 2, Casp3↑, 3, Casp8↑, 1, Casp9↑, 4, Cyt‑c↓, 1, Cyt‑c↑, 2, DR5↑, 1, Fas↑, 1, FasL↑, 1, Ferroptosis↑, 1, HGF/c-Met↓, 1, IAP1↓, 1, iNOS↓, 1, JNK↓, 1, JNK↑, 2, MAPK↓, 3, Mcl-1↓, 1, MDM2↓, 1, survivin↓, 1, Telomerase↓, 1, TumCD↑, 2,
Kinase & Signal Transduction ⓘ
HCAR2↑, 1, Sp1/3/4↓, 1,
Transcription & Epigenetics ⓘ
other?, 1, other↓, 33, other↑, 1, other↝, 6, tumCV↓, 1,
Protein Folding & ER Stress ⓘ
ER Stress↑, 1, HSP27↓, 1, HSP90↓, 1,
Autophagy & Lysosomes ⓘ
ATG5↑, 1, Beclin-1↑, 1, LC3‑Ⅱ/LC3‑Ⅰ↑, 1, LC3I↑, 1, LC3II↑, 1, TumAuto↓, 1, TumAuto↑, 3,
DNA Damage & Repair ⓘ
ATM↑, 1, DNAdam↑, 1, DNArepair↑, 1, DNMTs↓, 1, P53↑, 5, PARP↑, 1, γH2AX↑, 1,
Cell Cycle & Senescence ⓘ
CycB/CCNB1↓, 1, cycD1/CCND1↓, 1, RB1↑, 1, TumCCA↑, 4,
Proliferation, Differentiation & Cell State ⓘ
CD44↓, 1, EMT↓, 1, EMT↑, 1, ERK↓, 2, ERK↑, 1, p‑ERK↓, 1, FOXO3↑, 1, HDAC↓, 2, IGF-1R↓, 1, mTOR↓, 2, PI3K↓, 1, PTEN↑, 2, RAS↓, 1, TumCG↓, 5,
Migration ⓘ
Ca+2↑, 1, E-cadherin↑, 2, FAK↓, 1, KRAS↓, 1, MMP1↓, 1, MMP13↓, 1, MMP2↓, 1, MMP3↓, 1, MMP9↓, 2, MMPs↓, 2, N-cadherin↓, 1, Rho↓, 1, ROCK1↓, 1, Snail↓, 1, SOX4↓, 1, TGF-β↓, 2, TIMP1↑, 1, TumCI↓, 3, TumCMig↓, 2, TumCP↓, 5, TumMeta↓, 1, uPA↓, 2, β-catenin/ZEB1↓, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 2, EGFR↓, 1, EGR4↓, 1, Hif1a↓, 1, Hif1a↑, 1, VEGF↓, 1,
Barriers & Transport ⓘ
SLC12A5↝, 1,
Immune & Inflammatory Signaling ⓘ
CD4+↓, 1, COX2↓, 4, HCAR2↑, 1, IFN-γ↓, 1, IL1↓, 1, IL2↓, 1, IL4↓, 1, IL6↓, 1, Imm↑, 2, Inflam↓, 1, MCP1↓, 1, NF-kB↓, 4, NK cell↑, 1, PGE2↓, 1, TNF-α↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 2, BioAv↝, 1, ChemoSen↑, 8, Dose↝, 3, eff↓, 2, eff↑, 8, eff↝, 2, Half-Life↓, 1, RadioS↑, 1,
Clinical Biomarkers ⓘ
EGFR↓, 1, GutMicro↑, 1, IL6↓, 1, KRAS↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 3, AntiTum↑, 2, chemoP↑, 1, chemoPv↑, 2, OS?, 1, QoL↑, 1, RenoP↑, 1, Risk↓, 3, toxicity↓, 1,
Total Targets: 180
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 10, Catalase↑, 5, GPx↑, 4, GPx1↑, 1, GSH↑, 2, HO-1↓, 1, HO-1↑, 1, Iron↓, 1, lipid-P↓, 4, MDA↓, 4, NRF2↑, 3, RNS↓, 1, ROS↓, 14, ROS∅, 1, mt-ROS↓, 1, SIRT3↑, 1, SOD↓, 1, SOD↑, 4, SOD1↑, 1, SOD2↑, 1,
Metal & Cofactor Biology ⓘ
IronCh↑, 1,
Core Metabolism/Glycolysis ⓘ
GlucoseCon↑, 1, LDL↓, 2, NADPH↓, 1, PPARα↑, 1, SIRT1↑, 1,
Cell Death ⓘ
Akt↓, 1, Akt↑, 1, Apoptosis↓, 1, iNOS↓, 1,
Kinase & Signal Transduction ⓘ
TRPV3↑, 1,
Transcription & Epigenetics ⓘ
Ach?, 1, Ach↑, 1, other?, 1, other↓, 29, other↑, 3, other↝, 1,
Protein Folding & ER Stress ⓘ
ER Stress↓, 1,
DNA Damage & Repair ⓘ
DNAdam↓, 1, P53↓, 1,
Cell Cycle & Senescence ⓘ
E2Fs↑, 1,
Proliferation, Differentiation & Cell State ⓘ
FOXO3↑, 1, IGF-1R↓, 1, mTOR↓, 1, mTOR↑, 1, PI3K↑, 1, PTEN↓, 1,
Migration ⓘ
5LO↓, 2, AntiAg↑, 2, AP-1↓, 1, MMP2↓, 1, ZO-1↑, 1,
Angiogenesis & Vasculature ⓘ
Hif1a↓, 1, NO↓, 2, PDGFR-BB↓, 1,
Barriers & Transport ⓘ
BBB?, 1, BBB↑, 2,
Immune & Inflammatory Signaling ⓘ
COX1↓, 1, COX2↓, 3, IL10↑, 1, IL1β↓, 3, IL6↓, 4, IL8↓, 1, Imm↑, 2, Inflam↓, 9, JAK↓, 1, NF-kB↓, 3, TLR4↓, 1, TNF-α↓, 3,
Synaptic & Neurotransmission ⓘ
AChE↓, 5, BChE↓, 2, BDNF↑, 1, ChAT↑, 1, monoA↑, 1,
Protein Aggregation ⓘ
Aβ↓, 1, BACE↓, 1, NLRP3↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 2, BioAv↑, 5, BioAv⇅, 1, BioAv↝, 3, Dose↝, 1, eff↑, 7, Half-Life↓, 1, Half-Life↝, 1,
Clinical Biomarkers ⓘ
BP↓, 2, GutMicro↑, 1, IL6↓, 4,
Functional Outcomes ⓘ
AntiCan↑, 2, AntiDiabetic↑, 2, cardioP↑, 4, chemoPv↑, 1, cognitive↑, 9, hepatoP↓, 1, memory↑, 5, Mood↑, 2, motorD↑, 2, neuroP↑, 7, Obesity↓, 1, Pain↓, 1, Risk↓, 2, Sleep↑, 1, toxicity↓, 4, Wound Healing↑, 2,
Infection & Microbiome ⓘ
Bacteria↓, 2, Diar↓, 1, Sepsis↓, 1,
Total Targets: 107
Scientific Paper Hit Count for: other, other
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include :
-low or high Dose
-format for product, such as nano of lipid formations
-different cell line effects
-synergies with other products
-if effect was for normal or cancerous cells
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:% Target#:767 State#:% Dir#:1
wNotes=on sortOrder:rid,rpid
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