AST Cancer Research Results

AST, Aspartate Aminotransferase: Click to Expand ⟱
Source:
Type:
AST (Aspartate Aminotransferase) is an enzyme found in various tissues throughout the body, including the liver, heart, muscles, kidneys, and brain. Elevated levels of AST in the blood can be an indicator of tissue damage or disease.
AST levels can be elevated in certain types of cancer.
Used as a clinical biomarker for Liver function


Scientific Papers found: Click to Expand⟱
6477- 1,8-Cin,    Protective effect of 1, 8-cineole (eucalyptol) against lead-induced liver injury by ameliorating oxidative stress and inflammation and modulating TLR4/MyD88/NF-κB signaling
- in-vivo, Nor, NA
*MDA↓, 1, 8-cineole prevented an increase in the malondialdehyde level, a decrease in the glutathione level, and a decrease in the activity of superoxide dismutase and glutathione peroxidase enzymes in the liver of rats treated with lead acetate.
*GSH↑,
*GPx↑,
*Inflam↓, prevented an increase in the expression of pro-inflammatory cytokines and significantly reduced the infiltration of inflammatory cells in the liver parenchyma.
*TLR4↓, 1, 8-cineole discouraged the increase in toll-like receptor 4 (TLR4), myeloid differentiation primary response 88 (MyD88), and nuclear factor kappa B (NF-κB) expression in the liver
*MyD88↓,
*NF-kB↓,
*AST↓, and stopped a rise in serum AST and ALT enzymes.
*ALAT↓,
*hepatoP↑, hepatoprotection is probably achieved by inhibiting TLR4/MyD88/NF-κB signaling.
*ROS↓, 8-cineole can prevent liver damage caused by lead acetate by reducing oxidative stress and inflammation.

4390- AgNPs,    Therapeutic Potential of Cucumis melo (L.) Fruit Extract and Its Silver Nanopartciles Against DEN-Induced Hepatocellular Cancer in Rats
- in-vivo, Liver, NA
hepatoP↑, Treatment with crude extract and silver nanoparticles of Cucumis melo fruit indicates that Cucumis melo fruit could have exerted its protective effect.
AST↓, AST ALT, ALP, LDH, GGT
ALAT↓,
ALP↓,

4385- AgNPs,    Hepatoprotective effect of engineered silver nanoparticles coated bioactive compounds against diethylnitrosamine induced hepatocarcinogenesis in experimental mice
- in-vitro, Liver, NA
hepatoP↑, hepatoprotective activity of silver nanoparticles (AgNPs) synthesized using aqueous extracts of Andrographis paniculata leaves (ApAgNPs) and Semecarpus anacardium nuts (SaAgNPs) against diethylnitrosamine (DEN) induced liver cancer in mice model
*AST↓, decreased level of aspartate amino transferase (AST), alanine amino transferase (ALT), serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT) activity
*ALAT↓,
*Catalase↑, and elevated level of catalase (CAT), glutathione peroxidase (GPx), glutathione S-transferase (GST) and superoxide dismutase (SOD) activity
*GPx↑,
*GSTA1↑,
*SOD↑,

2206- AgNPs,  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
*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.
*Inflam↓,
*NF-kB↓,
*VEGF↓,
*SIRT1↑, Both RV and AgNPs + RV treatments increased SIRT1 levels, suggesting a potential role of SIRT1 activation in mediating the protective effects.
*ROS↓, alleviating sepsis-induced liver injury by modulating inflammation, oxidative stress, and endothelial dysfunction, potentially mediated through SIRT1 activation.
*Dose↝, 30 mg/kg of AgNPs + RV was given intraperitoneally to the rats
*Catalase↑, AgNPs + RV treatment exhibited a robust effect in bolstering CAT activity
*MDA↓, AgNPs + RV treatment effectively ameliorates sepsis-induced oxidative stress and inflammation in rat livers by reducing MDA, MPO, and NO levels
*MPO↓,
*NO↓,
*ALAT↓, AgNPs + RV effectively reduced the ALT and AST levels, returning them to values similar to those observed in the Sham group
*AST↓,
*antiOx↑, corroborates the antioxidant potential of RV and AgNPs observed in earlier studies

2660- AL,    Allicin: A review of its important pharmacological activities
- Review, AD, NA - Review, Var, NA - Review, Park, NA - Review, Stroke, NA
*Inflam↓, It showed neuroprotective effects, exhibited anti-inflammatory properties, demonstrated anticancer activity, acted as an antioxidant, provided cardioprotection, exerted antidiabetic effects, and offered hepatoprotection.
AntiCan↑,
*antiOx↑,
*cardioP↑, This vasodilatory effect helps protect against cardiovascular diseases by reducing the risk of hypertension and atherosclerosis.
*hepatoP↑,
*BBB↑, This allows allicin to easily traverse phospholipid bilayers and the blood-brain barrier
*Half-Life↝, biological half-life of allicin is estimated to be approximately one year at 4°C. However, it should be noted that its half-life may differ when it is dissolved in different solvents, such as vegetable oil
*H2S↑, allicin undergoes metabolism in the body, leading to the release of hydrogen sulfide (H2S)
*BP↓, H2S acts as a vasodilator, meaning it relaxes and widens blood vessels, promoting blood flow and reducing blood pressure.
*neuroP↑, It acts as a neuromodulator, regulating synaptic transmission and neuronal excitability.
*cognitive↑, Studies have suggested that H2S may enhance cognitive function and protect against neurodegenerative diseases like Alzheimer's and Parkinson's by promoting neuronal survival and reducing oxidative stress.
*neuroP↑, various research studies suggest that the neuroprotective mechanisms of allicin can be attributed to its antioxidant and anti-inflammatory properties
*ROS↓,
*GutMicro↑, may contribute to the overall health of the gut microbiota.
*LDH↓, Liu et al. found that allicin treatment led to a significant decrease in the release of lactate dehydrogenase (LDH),
*ROS↓, allicin's capacity to lower the production of reactive oxygen species (ROS), decrease lipid peroxidation, and maintain the activities of antioxidant enzymes
*lipid-P↓,
*antiOx↑,
*other↑, allicin was found to enhance the expression of sphingosine kinases 2 (Sphk2), which is considered a neuroprotective mechanism in ischemic stroke
*PI3K↓, allicin downregulated the PI3K/Akt/nuclear factor-kappa B (NF-κB) pathway, inhibiting the overproduction of NO, iNOS, prostaglandin E2, cyclooxygenase-2, interleukin-6, and tumor necrosis factor-alpha induced by interleukin-1 (IL-1)
*Akt↓,
*NF-kB↓,
*NO↓,
*iNOS↓,
*PGE2↓,
*COX2↓,
*IL6↓,
*TNF-α↓, Allicin has been found to regulate the immune system and reduce the levels of TNF-α and IL-8.
*MPO↓, Furthermore, allicin significantly decreased tumor necrosis factor-alpha (TNF-α) levels and myeloperoxidase (MPO) activity, indicating its neuroprotective effect against brain ischemia via an anti-inflammatory pathway
*eff↑, Allicin, in combination with melatonin, demonstrated a marked reduction in the expression of nuclear factor erythroid 2-related factor 2 (Nrf-2), Kelch-like ECH-associated protein 1 (Keap-1), and NF-κB genes in rats with brain damage induced by acryl
*NRF2↑, Allicin treatment decreased oxidative stress by upregulating Nrf2 protein and downregulating Keap-1 expression.
*Keap1↓,
*TBARS↓, It significantly reduced myeloperoxidase (MPO) and thiobarbituric acid reactive substances (TBARS) levels,
*creat↓, and decreased blood urea nitrogen (BUN), creatinine, LDH, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and malondialdehyde (MDA) levels.
*LDH↓,
*AST↓,
*ALAT↓,
*MDA↓,
*SOD↑, Allicin also increased the activity of superoxide dismutase (SOD) as well as the levels of glutathione S-transferase (GST) and glutathione (GSH) in the liver, kidneys, and brain
*GSH↑,
*GSTs↑,
*memory↑, Allicin has demonstrated its ability to improve learning and memory deficits caused by lead acetate injury by promoting hippocampal astrocyte differentiation.
chemoP↑, Allicin safeguards mitochondria from damage, prevents the release of cytochrome c, and decreases the expression of pro-apoptotic factors (Bax, cleaved caspase-9, cleaved caspase-3, and p53) typically activated by cisplatin
IL8↓, Allicin has been found to regulate the immune system and reduce the levels of TNF-α and IL-8.
Cyt‑c↑, In addition, allicin was reported to induce cytochrome c, increase expression of caspase 3 [86], caspase 8, 9 [82,87], caspase 12 [80] along with enhanced p38 protein expression levels [81], Fas expression levels [82].
Casp3↑,
Casp8↑,
Casp9↑,
Casp12↑,
p38↑,
Fas↑,
P53↑, Also, significantly increased p53, p21, and CHK1 expression levels decreased cyclin B after allicin treatment.
P21↑,
CHK1↓,
CycB/CCNB1↓,
GSH↓, Depletion of GSH and alterations in intracellular redox status have been found to trigger activation of the mitochondrial apoptotic pathway was the antiproliferative function of allicin
ROS↑, Hepatocellular carcinoma (HCC) cells were sensitised by allicin to the mitochondrial ROS-mediated apoptosis induced by 5-fluorouracil
TumCCA↑, According to research findings, allicin has been shown to decrease the percentage of cells in the G0/G1 and S phases [87], while causing cell cycle arrest at the G2/M phase
Hif1a↓, Allicin treatment was found to effectively reduce HIF-1α protein levels, leading to decreased expression of Bcl-2 and VEGF, and suppressing the colony formation capacity and cell migration rate of cancer cells
Bcl-2↓,
VEGF↓,
TumCMig↓,
STAT3↓, antitumor properties of allicin have been attributed to various mechanisms, including promotion of apoptosis, inhibition of STAT3 signaling
VEGFR2↓, suppression of VEGFR2 and FAK phosphorylation
p‑FAK↓,

3446- ALA,  CUR,    The Potential Protective Effect of Curcumin and α-Lipoic Acid on N-(4-Hydroxyphenyl) Acetamide-induced Hepatotoxicity Through Downregulation of α-SMA and Collagen III Expression
- in-vivo, Nor, NA
*hepatoP↑, Curc and Lip acid can be considered as promising natural therapies against liver injury, induced by NHPA, through their antioxidant and antifibrotic actions.
*α-SMA↓, Curc and Lip acid reduced the expression of alpha-smooth muscle actin and collagen III, upregulated by NHPA intoxication
*COL3A1↓,
*ROS↓, scavenging activity to ROS and a capacity to regenerate endogenous antioxidants such as GSH, and vitamins C and E.
*GSH↑,
*ALAT↓, ALT, AST, and ALP activity levels compared to those of the control group. The use of NACS, Curc, and/or Lip acid significantly reduced the toxic effects of NHPA on those enzymes,
*AST↓,
*ALP↓,
*MDA↓, The combination therapy showed an apparent reduction in MDA level more than other treatments

3164- Ash,    Withaferin A alleviates fulminant hepatitis by targeting macrophage and NLRP3
*hepatoP↑, Withania Somnifera, is a hepatoprotective agent
*IKKα↓, WA also inhibits inflammation by directly inhibiting IκκB activity46,47 or NLRP3 inflammasome activation in vitro in immune cells
*NLRP3↓,
*NRF2↑, WA probably protects against FH by targeting the macrophage and/or hepatocyte stress via activating NRF2, AMPKα
*AMPK↑,
*Inflam↓, Thus, WA potently protects against GalN/LPS-induced hepatotoxicity and inflammation
*Apoptosis↓, WA suppressed hepatic apoptosis in vivo
*cl‑Casp3↓, attenuate the increase of cleaved CASP3 and cleaved PARP1
*cl‑PARP1↓,
*NLRP3↓, WA prevented GalN/LPS-induced FH partially by inhibiting activation of the NLRP3 inflammasome
*ROS↓, fig 7
*ALAT↓,
*AST↓,
*GSH↑, (GSH) levels were significantly depleted by ~50% 6 h after GalN/LPS administration and were recovered to levels comparable with that of control mice by WA treatment

5506- Ba,    Improved Bioavailability and Hepatoprotective Activity of Baicalein Via a Self-assembled Solutol HS15 Micelles System
- in-vivo, Nor, NA
*AST↓, The in vivo results showed that HS15-BA micelles significantly inhibited the activity of the CCl4-induced liver injury marker enzymes aspartate transaminase (AST) and alanine transaminase (ALT).
*ALAT↓,
*GSH↓, leading to increased L-glutathione (GSH) and superoxide dismutase (SOD) activity and decreased malondialdehyde (MDA) activity, while HS15-BA significantly reversed the above changes.
*SOD↓,
*MDA↓,
*hepatoP↑, BA also had a hepatoprotective effect through anti-inflammatory activity;
*Inflam↓,
BioAv↑, In summary, our study confirmed that HS15-BA micelles enhanced the bioavailability of BA, and showed hepatoprotective effects through antioxidant and anti-inflammatory activities.

2626- Ba,    Molecular targets and therapeutic potential of baicalein: a review
- Review, Var, NA - Review, AD, NA - Review, Stroke, NA
AntiCan↓, anticancer, antidiabetic, antimicrobial, antiaging, neuroprotective, cardioprotective, respiratory protective, gastroprotective, hepatic protective, and renal protective effects
*neuroP↑,
*cardioP↑, Cardioprotective action of baicalein
*hepatoP↑,
*RenoP↑, baicalein’s capacity to lessen cisplatin-induced nephrotoxicity is probably due, at least in part, to the attenuation of renal oxidative and/or nitrative stress
TumCCA↑, Baicalein induces G1/S arrest in lung squamous carcinoma (CH27) cells by downregulating CDK4 and cyclin D1, as well as upregulating cyclin E
CDK4↓,
cycD1/CCND1↓,
cycE/CCNE↑,
BAX↑, SGC-7901 cells showed that when baicalein was administered, Bcl-2 was downregulated and Bax was increased
Bcl-2↓,
VEGF↓, Baicalein inhibits the synthesis of vascular endothelial growth factor (VEGF), HIF-1, c-Myc, and nuclear factor kappa B (NF-κB) in the G1 and S phases of ovarian cancer cell
Hif1a↓,
cMyc↓,
NF-kB↓,
ROS↑, Baicalein produced intracellular reactive oxygen species (ROS) and activated BNIP3 to slow down the development and hasten the apoptosis of MG-63,OS cell
BNIP3↑,
*neuroP↑, Baicalein exhibits neuroprotective qualities against amyloid (AN) functions by preventing AN from aggregating in PC12 neuronal cells to cause A𝛽-induced cytotoxicity
*cognitive↑, baicalein encourages non-amyloidogenic processing of APP, which lowers the generation of A𝛽 and enhances cognitive function
*NO↓, baicalein effectively reduced NO generation and iNOS gene expression
*iNOS↓,
*COX2↓, Baicalein therapy significantly decreased the expression of COX-2 and iNOS, as well as PGE2 and NF-κB, indicating a protective effect against cerebral I/R injury.
*PGE2↓,
*NRF2↑, Baicalein therapy markedly elevated nuclear Nrf2 expression and AMPK phosphorylation in the ischemic cerebral cortex
*p‑AMPK↑,
*Ferroptosis↓, Baicalein suppressed ferroptosis associated with 12/15-LOX, hence lessening the severity of post-traumatic epileptic episodes generated by FeCl3
*lipid-P↓, HT22 cells were damaged by ferroptosis, which is mitigated by baicalein may be due to its lipid peroxidation inhibitor
*ALAT↓, Baicalin lowers the raised levels of hepatic markers alanine transaminase (ALT), aspartate aminotransferase (AST)
*AST↓,
*Fas↓, Baicalin has also been shown to suppress apoptosis, decrease FAS protein expression, block the caspase-8 pathway, and decrease Bax protein production
*BAX↓,
*Apoptosis↓,

2613- Ba,    Hepatoprotective Effect of Baicalein Against Acetaminophen-Induced Acute Liver Injury in Mice
- in-vivo, Nor, NA
*hepatoP↑, baicalein significantly ameliorated APAP-exposed liver damage and histological hepatocyte changes
*MDA↓, baicalein (50 or 100 mg/kg) pretreatment significantly inhibited liver MDA level (p < 0.05; Figure 4), increased SOD, CAT and GSH activity.
*SOD↑,
*Catalase↑,
*GSH↑,
*MAPK↓, Baicalein Prevented the MAPK Pathway Activation
*p‑JAK2↓, BAI Suppressed the Expression of p-JAK2 and p-STAT3 Proteins in APAP Liver Injury
*p‑STAT3↓,
*ALAT↓, our experimental results suggested that serum ALT and AST levels were obviously alleviated by Baicalein in a dose-dependent manner
*AST↓,
*ROS↓, hepatoprotective role of BAI via attenuating oxidative stress
*antiOx↑, hepatoprotective activity of Baicalein might be associated with its antioxidative capacity.

2677- BBR,    Liposome-Encapsulated Berberine Alleviates Liver Injury in Type 2 Diabetes via Promoting AMPK/mTOR-Mediated Autophagy and Reducing ER Stress: Morphometric and Immunohistochemical Scoring
- in-vivo, Diabetic, NA
*hepatoP↑, berberine (Lip-BBR) to aid in ameliorating hepatic damage and steatosis, insulin homeostasis, and regulating lipid metabolism in type 2 diabetes (T2DM)
*LC3II↑, Lip-BBR treatment promoted autophagy via the activation of LC3-II and Bclin-1 proteins and activated the AMPK/mTOR pathway in the liver tissue of T2DM rats.
*Beclin-1↑,
*AMPK↑,
*mTOR↑,
*ER Stress↓, It decreased the endoplasmic reticulum stress by limiting the CHOP, JNK expression, oxidative stress, and inflammation.
*CHOP↓,
*JNK↓,
*ROS↓,
*Inflam↓,
*BG↓, Oral supplementation of diabetic rats either by Lip-BBR or Vild, 10 mg/kg of each, significantly (p < 0.001) lowered the blood glucose levels of tested diabetic rats compared to the diabetic group.
*SOD↑, when the diabetic rats received Lip-BBR, the decrements were less pronounced compared to the diabetic group by 1.16 fold, 2.52 fold, and 67.57% for SOD, GPX, and CAT, respectively.
*GPx↑,
*Catalase↑,
*IL10↑, Treatment of the diabetic rats with Lip-BBR significantly (p < 0.001) elevated serum IL-10 levels by 37.01% compared with diabetic rats.
*IL6↓, Oral supplementation of Lip-BBR could markedly (p < 0.0001) reduce the elevated serum levels of IL-6 and TNF-α when it is used as a single treatment by 55.83% and 49.54%,
*TNF-α↓,
*ALAT↓, ALT, AST, and ALP in the diabetic group were significantly higher (p < 0.0001) by 88.95%, 81.64%, and 1.8 fold, respectively, compared with those in the control group, but this was reversed by the treatment with Lip-BBR
*AST↓,
*ALP↓,

5633- BCA,    Mechanisms Behind the Pharmacological Application of Biochanin-A: A review
- Review, Var, NA - Review, AD, NA
*AntiDiabetic↑, Through modulating oxidative stress, SIRT-1 expression, PPAR gamma receptors, and other multiple mechanisms biochanin-A produces anti-diabetic action.
*neuroP↑, Biochanin-A has been shown to have a potential neuroprotective impact by modulating multiple critical neurological pathways.
*toxicity↓, Unlike chemical agents such as chemotherapeutic agents, isoflavones have shown zero toxicity to humans
*CYP19↓, Biochanin-A inhibits CYP19 and negatively affects the synthesis of oestrogen in the body which enhances the anti-oestrogenic property in hormone-influenced cancer such as prostate cancer and breast cancer
p‑Akt↓, Biochanin-A inhibits Akt phosphorylation thereby downregulates mTOR signals and disrupts the cell cycle.
mTOR↓,
TumCCA↑,
P21↑, Biochanin-A cause apoptosis in lung cancer by increasing p21, caspase-3, and Bcl-2 levels. It lowers E-cadherin and blocks metastasis.
Casp3↑,
Bcl-2↑,
Apoptosis↑,
E-cadherin↓,
TumMeta↓,
eff↑, The synergism of biochanin-A with 5-fluorouracil evidenced in Caco-2 and HCT-116 cell lines indicates the modulatory influence of biochanin-A in colon cancer treatment.
GSK‐3β↓, It blocked the “Akt and GSK3β phosphorylation and boosted the degradation of β-catenin” ( Mahmoud et al., 2017).
β-catenin/ZEB1↓,
RadioS↑, Biochanin-A when combined with gamma radiation on HT29 cells, which is resistant to radiation, had revealed a reduction in cell proliferation.
ROS↑, Raised levels of ROS, lipid peroxidation, MMP, caspase-3 have been observed more in the treatment group with significant apoptosis
Casp1↑,
MMP2↓, biochanin-A influenced the tumour invasion capacity by lowering matrix-degrading enzymes (MMP 2 and MMP 9) tested in U87MG cells
MMP9↓,
EGFR↓, Biochanin-A by lowering EGFR, p-ERK (Extracellular signal related kinases), p-AKT (Protein kinase-B), c-myc, and MT-MMP1 (Membrane type matrix metalloproteinase) activation, inhibited cell survival.
ChemoSen↑, Biochanin-A synergistically improved temozolomide anti-cancer ability in GBM
PI3K↓, Cell signalling pathways MAP kinase, PI3 kinase, mTOR, matrix metalloproteases, hypoxia-inducible factor, and VEGF were inhibited by biochanin-A, making it suitable in treating GBM
MMPs↓,
Hif1a↓,
VEGF↓,
*ROS↓, anti-diabetic mechanism of biochanin-A is by decreasing oxidative stress
*Obesity↓, strongly suggest that biochanin-A has therapeutic potential in the treatment of obesity and the prevention of cardiovascular disease
*cardioP↑,
*NRF2↑, Biochanin-A up-regulated the Nrf-2 pathway while suppressing the NF-κB cascade,
*NF-kB↓, By activating the Nrf-2 pathway and inhibiting NF-κB activation, biochanin-A may reduce obesity and its related cardiomyopathy by decreasing oxidative stress and inflammation
*Inflam↓,
*lipid-P↓, cardio-protective effects by controlling lipid peroxidation
*hepatoP↑, biochanin-A influence the elevated hepatic enzyme level, such as AST, ALP, ALT, bilirubin, etc., and found to be a promising molecule in hepatotoxicity models
*AST↓,
*ALP↓,
*Bacteria↓, The results indicate that biochanin-A may be an effective alternate to antibiotics for alleviating SARA in cattles
*neuroP↑, the neuroprotective effects of biochanin-A might be attributed to the activation of the Nrf2 pathway and suppression of the NF-κB pathway
*SOD↑, Biochanin-A reduced oxidative stress in the brain by augmenting SOD (superoxide dismutase) and GSH-Px (glutathione peroxidase) and repressing MDA (malondialdehyde) levels.
*GPx↑,
*AChE↓, Acetylcholinesterase activity was found decreased in a dose-reliant manner amongst biochanin-A treated animals
*BACE↓, Biochanin-A non-competitively inhibited BACE1 with an IC 50 value of 28 μM.
*memory↑, estore learning and memory deficits in ovariectomized (OVX) rats.
*BioAv↓, The bioavailability of biochanin-A is poor.

2760- BetA,    A Review on Preparation of Betulinic Acid and Its Biological Activities
- Review, Var, NA - Review, Stroke, NA
AntiTum↑, BA is considered a future promising antitumor compound
Cyt‑c↑, BA stimulated mitochondria to release cytochrome c and Smac and cause further apoptosis reactions
Smad1↑,
Sepsis↓, Administration of 10 and 30 mg/kg of BA significantly improved survival against sepsis and attenuated lung injury.
NF-kB↓, BA inhibited nuclear factor-kappa B (NF-κB) expression in the lung and decreased levels of cytokine, intercellular adhesion molecule-1 (ICAM-1), monocyte chemoattractant protein-1 (MCP-1) and matrix metalloproteinase-9 (MMP-9)
ICAM-1↓,
MCP1↓,
MMP9↓,
COX2↓, In hPBMCs, BA suppressed cyclooxygenase-2 (COX-2) expression and prostaglandin E2 (PEG2) production by inhibiting extracellular regulated kinase (ERK) and Akt phosphorylation and thereby modulated the NF-κB signaling pathway
PGE2↓,
ERK↓,
p‑Akt↓,
*ROS↓, BA significantly decreased the mortality of mice against endotoxin shock and inhibited the production of PEG2 in two of the most susceptible organs, lungs and livers [80]. Moreover, BA reduced reactive oxygen species (ROS) formation
*LDH↓, and the release of lactate dehydrogenase
*hepatoP↑, hepatoprotective effect of BA from Tecomella undulata.
*SOD↑, Pretreatment of BA prevented the depletion of hepatic antioxidants superoxide dismutase (SOD) and catalase (CAT), reduced glutathione (GSH) and ascorbic acid (AA) and decreased the CCl4-induced LPO level
*Catalase↑,
*GSH↑,
*AST↓, A also attenuated the elevation of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) plasma level,
*ALAT↓,
*RenoP↑, BA also exhibits renal-protective effects. Renal fibrosis is an end-stage renal disease symptom that develops from chronic kidney disease (CKD).
*ROS↓, BA protected against this ischemia-reperfusion injury in a mice model by enhancing blood flow and reducing oxidative stress and nitrosative stress
*α-SMA↓, Moreover, BA reduced the expression of α-smooth muscle actin (α-SMA) and collagen-I

3517- Bor,  Se,    The protective effects of selenium and boron on cyclophosphamide-induced hepatic oxidative stress, inflammation, and apoptosis in rats
- in-vivo, Nor, NA
*hepatoP↑, However, it was found that Se protects the liver slightly better against CP damage than B
*ALAT↓, statistically significant difference was observed in the serum levels of ALT, AST, ALP, TAS, TOS and OSI.
*AST↓,
*ALP↓,
*NF-kB↓, A statistically significant difference was observed in serum levels of NF-kB, TNF-α, IL -1β, IL -6 and IL -10 when the Se + CP and B + CP-treated groups were compared with the CP-treated group
*TNF-α↓, fig 9
*IL1β↓,
*IL6↓,
*IL10↑,
*SOD↑, A statistically remarkable change in serum levels of SOD, CAT, GPx, MDA and GSH was observed in the group receiving only CP compared to groups Se, B and the control.
*Catalase↑,
*MDA↓, Fig 10
*GSH↑,
*GPx↑,
*antiOx↑, suggests that B and Se increase intracellular antioxidant status.
*NRF2↑, Se and B treatment can protect rat liver tissue from CP-induced oxidative stress, inflammation, and apoptosis by regulating Bax/Bcl-2 and Nrf2-Keap-1 signaling pathways.
*Keap1↓,

3510- Bor,    Boron Affects the Development of the Kidney Through Modulation of Apoptosis, Antioxidant Capacity, and Nrf2 Pathway in the African Ostrich Chicks
- in-vivo, Nor, NA
*RenoP↑, Our results revealed that low doses of boron (up to 160 mg) had positive effect, while high doses (especially 640 mg) caused negative effect on the development of the kidney
*ROS↓, The low doses regulate the oxidative and enzyme activity in the kidney.
*antiOx↑, boron at low doses upregulated the expression of genes involved in the antioxidant pathway
*Apoptosis↓, low levels of boron (up to 160 mg) inhibited the cell apoptosis, regulate the enzyme activity, and improved the antioxidant system, thus may encourage the development of the ostrich chick's kidney
*NRF2↑, maximum localization of Nrf2 in 80 mg/L BA dose group
*HO-1↑, As the boron concentration increased, the expression of Nrf2, GCLc, and HO-1 genes upregulated
*MDA↓, In comparison to those of the group 1, MDA content (lipid peroxidation marker) was significantly decreased by 26.02 and 48.12% in the 40 and 80 mg/L BA groups
*lipid-P↓,
*GPx↓, GSH-PX activity of ostrich chick kidney tissue was slightly increased in the 40 and 80 mg/L BA groups,
*Catalase↑, supplementation of low doses of boron in the ostrich drinking water has resulted in stimulation of antioxidant capacity of GR, CAT, and SOD significantly.
*SOD↑,
*ALAT↓, boron supply in low doses (especially 80 mg/L BA) showed decrease levels in the activity of ALT, AST, and ALP.
*AST↓,
*ALP↓,

2775- Bos,    The journey of boswellic acids from synthesis to pharmacological activities
- Review, Var, NA - Review, AD, NA - Review, PSA, NA
ROS↑, modulation of reactive oxygen species (ROS) formation and the resulting endoplasmic reticulum stress is central to BA’s molecular and cellular anticancer activities
ER Stress↑,
TumCG↓, Cell cycle arrest, growth inhibition, apoptosis induction, and control of inflammation are all the effects of BA’s altered gene expression
Apoptosis↑,
Inflam↓,
ChemoSen↑, BA has additional synergistic effects, increasing both the sensitivity and cytotoxicity of doxorubicin and cisplatin
Casp↑, BA decreases viability and induces apoptosis by activat- ing the caspase-dependent pathway in human pancreatic cancer (PC) cell lines
ERK↓, BA might inhibit the activation of Ak strain transforming (Akt) and extracellular signal–regulated kinase (ERK)1/2,
cl‑PARP↑, initiation of cleavage of PARP were prompted by the treatment with AKBA
AR↓, AKBA affects the androgen receptor by reducing its expression,
cycD1/CCND1↓, decrease in cyclin D1, which inhibits cellular proliferation
VEGFR2↓, In prostate cancer, the downregulation of vascular endothelial growth factor receptor 2–mediated angiogenesis caused by BA
CXCR4↓, Figure 6
radioP↑,
NF-kB↓,
VEGF↓,
P21↑,
Wnt↓,
β-catenin/ZEB1↓,
Cyt‑c↑,
MMP2↓,
MMP1↓,
MMP9↓,
PI3K↓,
MAPK↓,
JNK↑,
*5LO↓, Table 1 (non cancer)
*NRF2↑,
*HO-1↑,
*MDA↓,
*SOD↑,
*hepatoP↑, Preclinical studies demonstrated hepatoprotective impact for BA against different models of hepatotoxicity via tackling oxidative stress, and inflammatory and apoptotic indices
*ALAT↓,
*AST↓,
*LDH↑,
*CRP↓,
*COX2↓,
*GSH↑,
*ROS↓,
*Imm↑, oral administration of biopolymeric fraction (BOS 200) from B. serrata in mice led to immunostimulatory effects
*Dose↝, BA at low concentration tend to stimulate an immune response, as those utilized in the study of Beghelli et al. (2017) however, utilizing higher concentration suppressed the immune response
*eff↑, Useful actions on skin and psoriasis
*neuroP↑, AKBA has substantially diminished the levels of inflammatory markers such as 5-LOX, TNF-, IL-6, and meliorated cognition in lipopolysaccharide-induced neuroinflammation rodent models
*cognitive↑,
*IL6↓,
*TNF-α↓,

6556- BSB,    A Comprehensive Study of Therapeutic Applications of Chamomile
- Review, Nor, NA - Review, AD, NA - Review, Park, NA - Review, Stroke, NA
*Inflam↓, anti-inflammatory, antioxidant, analgesic, antimicrobial, hepatoprotective, anti-allergic, anticancer, and anti-hypertensive agent
*antiOx↑,
*AntiBio↑,
*hepatoP↑,
*AntiCan↑,
*other↝, Two major species of chamomile widely used for health conditions are German chamomile (M. chamomilla L.) and Roman or English chamomile (Chamaemelum nobile syn. Anthemis nobilis L.) [6]
*toxicity↓, Chamomile is generally safe for consumption and is consumed as tea or tonic.
*Wound Healing↓, As a drug, it is useful in flatulence, colic, hysteria, intermittent fever, depression, ulcer, and wound healing
*Dose↝, The main constituents of the oil include terpenoids, mainly sesquiterpenes and α-bisabolol
*Dose↝, The major flavonoids present are apigenin, quercetin, patuletin, and luteolin in concentrations of 16.8%, 9.9%, 6.5%, and 1.9%, respectively, of course again depending on the species and cultivation.
*eff↝, The main components in German chamomile are terpenoid; α-bisabolol and its oxide azulenes, such as chamazulene (1–15%); and apigenin [12,16,17,18]. Roman chamomile, on the other hand, contains mainly angelic acid and tiglic acid esters
*ROS↓, e herb significantly reduced reactive oxygen species (ROS) levels, with the most prominent effect witnessed at a dose of 1000 mg/mL.
*TNF-α↓, significant reduction in TNF-α and IL-6 was observed, which suggests anti-inflammatory activities.
*IL6↓,
*other↝, Chamomile, being a natural antioxidant, possesses the ability to scavenge free radicals and, thus, can be effective for the management of neurological disorders such as Alzheimer’s disease, Parkinson’s disease, and cerebral ischemia
*AST↓, aqueous chamomile extracts reduced the levels of AST and ALT by 33–37%.
*ALAT↓,

5755- CA,    Caffeic Acid as a Promising Natural Feed Additive: Advancing Sustainable Aquaculture
- Review, Nor, NA
*Imm↑, CA enhances immune responses, reduces inflammation, exerts antimicrobial effects, and improves overall fish health.
*Inflam↓,
*Bacteria↓,
*eff↑, sustainable functional-feed strategies that diminish antibiotic reliance in aquaculture.
*ROS↓, Reduced MDA levels and ROS accumulation
*MDA↓,
*Catalase↑, Increased CAT, GSH, and T-AOC activities
*GSH↑,
*TAC↑,
*NF-kB↓, Suppressed the activation of the NF-κB signaling pathway and the NLRP3 inflammasome pathway in the gills
*NLRP3↓,
*eff↑, In rainbow trout (Oncorhynchus mykiss), co-supplementation with 1–3 g RA/kg and Lactobacillus rhamnosus yielded synergistic improvements in growth, antioxidant capacity, and stress tolerance
*AST↓, In rainbow trout, CinA (0.25–1.5 g/kg) lowered intestinal pH, serum triglycerides, and hepatic enzyme levels (AST and ALT), while upregulating hepatic antioxidant genes (SOD and GST) [49]
*ALAT↓,
*SOD↑,
*GSTA1↑,

5924- CA,    Carnosic acid impedes cell growth and enhances anticancer effects of carmustine and lomustine in melanoma
- vitro+vivo, Melanoma, B16-F10
TumCG↓, CA exhibits significant growth inhibition and cell cycle arrest in melanoma B16F10 cells.
TumCCA↑,
P21↑, CA triggers cell cycle arrest at G0/G1 phase, and enhances p21 expression.
eff↑, CA can enhance BCNU- and CCNU-mediated cytotoxicity and cell cycle arrest in B16F10 cells.
AST↓, reduces the values of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in vivo.
ALAT↓,

5887- CAR,  TV,    Antitumor Effects of Carvacrol and Thymol: A Systematic Review
- Review, Var, NA
Apoptosis↑, It was attested that carvacrol and thymol induced apoptosis, cytotoxicity, cell cycle arrest, antimetastatic activity,
TumCCA↑, accumulation of cells in the G1 phase, together with a reduction of cells in the S phase, slowing cell cycle/mitosis and provoking cell death.
TumMeta↓,
TumCP↓, antiproliferative effects and inhibition of signaling pathways (MAPKs and PI3K/AKT/mTOR).
MAPK↓,
PI3K↓,
Akt↓,
mTOR↓,
eff↑, carvacrol appears to be more potent than thymol
*Inflam↓, these compounds present anti-inflammatory (Li et al., 2018; Chamanara et al., 2019) and antioxidant
*antiOx↑,
AXL↓, These effects occurred mainly through the inhibition of tyrosine kinase receptor (AXL) expression and an increase in malondialdehyde (MDA
MDA↑,
Casp3↑, caspase-3 activation and Bcl-2 inhibition
Bcl-2↓,
MMP2↓, promoted a decrease in Bcl-2, metalloproteinase-2 and -9 (MMP-2 and MMP-9), p-ERK, p-Akt, cyclin B1 levels and an increase in p-JNK, Bax levels, resulting in cell cycle arrest at the G2/M phase
MMP9↓,
p‑JNK↑,
BAX↑,
MDA↓, In respect of breast cancer, treatment with carvacrol decreases MDA-MB231 (Jamali et al., 2018; Li et al., 2021) and MCF-7 cells line viability
TRPM7↓, TRPM7 pathway is one of the suggested pharmacological mechanisms of action
MMP↓, decreased mitochondrial membrane potential, cytochrome C release, caspase activation, PARP cleavage
Cyt‑c↑,
Casp↑,
cl‑PARP↑,
ROS↑, Carvacrol also induced cytotoxicity and apoptosis (via caspase-3 and reactive oxygen species—ROS) of human oral squamous cell carcinoma (OC2 cell line)
CDK4↓, In tongue cancer (Tca-8113, SCC-25 cell lines), Dai et al. (2016) reported that carvacrol effectively inhibited cell proliferation through the negative regulation of CCND1 and CDK4 expression, and the positive regulation of p21 expression,
P21↑,
F-actin↓, A blockade of TRPM7 channels, reduced expression of MMP-2 and F-actin, was also observed, together with the inhibition of PI3K/Akt and MAPK
GSH↓, by increasing ROS, Bax, Caspase-3, -9 levels and reducing Bcl-2 and GSH levels.
*SOD↑, Moreover, carvacrol was able to increase the levels of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione (GSH), along with a reduction of lipid peroxides and the enzymes AST, ALT, AL
*Catalase↑,
*GPx↑,
*GSR↑,
*GSH↑,
*lipid-P↓,
*AST↓,
*ALAT↓,
*ALP↓,
*LDH↓,
DNAdam↑, hepatocellular carcinoma induced by diethylnitrosamine (DEN), carvacrol treatment promoted DNA fragmentation
AFP↓, carvacrol showed a reduction in serum levels of alpha-fetoprotein (AFP), alpha l-fucosidase (AFU), vascular endothelial growth factor (VEGF
VEGF↓,
Weight↑, Carvacrol supplementation significantly improved the weight gain and growth rate of animals with colon cancer
*chemoP↑, reduction in oxidative stress damage (higher levels of GSH, GPx, GR, SOD and CAT), suggesting that carvacrol presents chemopreventive effects
ROS↑, In vitro, carvacrol and thymol increased the generation of reactive oxygen species in 24.63% (n = 17) of the studies, a fact that is also observed in chemotherapeutics

5888- CAR,    Therapeutic application of carvacrol: A comprehensive review
- Review, Var, NA - Review, Stroke, NA - Review, Diabetic, NA - Review, Park, NA
*antiOx↑, demonstrated as anti‐oxidant, anticancer, diabetes prevention, cardioprotective, anti‐obesity, hepatoprotective and reproductive role, antiaging, antimicrobial, and immunomodulatory properties.
*AntiCan↑,
*AntiDiabetic↑,
*cardioP↑,
*Obesity↓,
*hepatoP↑,
*AntiAg↑,
*Bacteria↓,
*Imm↑,
MMP2↓, anticancer ability against malignant cells via decreasing the expressions of matrix metalloprotease 2 and 9, inducing apoptosis
MMP9↓,
Apoptosis↓,
MMP↓, disrupting mitochondrial membrane, suppressing extracellular signal‐regulated kinase 1/2 mitogen‐activated protein kinase signal transduction
ERK↓,
PI3K↓, decreasing the phosphoinositide 3‐kinase/protein kinase B.
ALAT↓, decreased the concentrations of alanine aminotransferase, alkaline phosphatase and aspartate aminotransferase,
*ROS↓, Essential oils found in plants are natural anti‐oxidants that reduce cell damage caused by reactive species and prevent mutagenic and carcinogenic processes.
*Catalase↑, Carvacrol has remarkably higher anti‐oxidative and hepatoprotective properties, which improves the activity of enzymatic anti‐oxidants (catalase, superoxide dismutase, and glutathione peroxidase)
*SOD↑,
*GPx↑,
*AST↓, Carvacrol decreased the level of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactic acid dehydrogenase (LDH) and improved the status of inflammation, necrosis, and coagulation in the liver
*LDH↓,
*necrosis↓,
ROS↑, prostate cancer cells via lowering cell viability, increasing the rate of reactive oxygen species, and disrupting the mitochondrial membrane potential.
TumCCA↑, Carvacrol induced cell cycle arrest at G0/G1 that declined increased CDK inhibitor p21 expression and decreased cyclin‐dependent kinase 4 (CDK4), and cyclin D1 expressions.
CDK4↓,
cycD1/CCND1↓,
NOTCH↓, carvacrol inhibited Notch signaling in PC‐3 cells via downregulating Jagged‐1 and Notch‐1
IL6↓, human prostate cancer cell lines, which significantly reduced IL‐6
chemoP↑, Carvacrol has significant protective effects in reducing the side effects of chemotherapeutics such as irinotecan hydrochloride anticancer drugs that cause induction of intestinal mucositis.
*Pain↓, Pain management
*neuroP↑, The neuroprotective role of carvacrol was examined by Guan et al. in 2019 against ischemic stroke,
*TRPM7↓, downregulating TRPM7 channels
*motorD↑, improved catalepsy, akinesia, bradykinesia, locomotor activity, and motor coordination.
*NF-kB↓, Carvacrol reduced inflammatory biomarkers, such as nuclear factor κB and cyclooxygenase‐2, and levels of nitric oxides, malondialdehyde, and glutathione create oxidative stress.
*COX2↓,
*MDA↓,

5909- CAR,    Potential preventive effect of carvacrol against diethylnitrosamine-induced hepatocellular carcinoma in rats
*AST↓, Carvacrol supplementation (15 mg/kg body weight) significantly attenuated these alterations, thereby showing potent anticancer effect in liver cancer
*ALAT↓,
*ALP↓,
*LDH↓,
*SOD↑,
*Catalase↑,
*GSH↑,
*GPx↑,
*GSR↑,
*hepatoP↑, These findings suggest that carvacrol prevents lipid peroxidation, hepatic cell damage, and protects the antioxidant system in DEN-induced hepatocellular carcinogenesis.
*lipid-P↓,

5898- CAR,    Carvacrol-induced apoptosis via tumor suppressor gene activation and oxidative stress modulation in a rat model of breast cancer
- in-vivo, BC, NA
*lipid-P↓, Carvacrol also attenuated lipid peroxidation by reducing malondialdehyde (MDA) levels, while boosting total antioxidant capacity and improving inflammatory status.
*MDA↓,
*antiOx↑,
*Inflam↑,
RenoP↑, Moreover, restoration of liver and kidney function was observed through normalization of serum ALT, AST, urea, and creatinine levels
hepatoP↑,
*ALAT↓,
AST↓,
creat↓,
chemoPv↑, Preclinical studies have demonstrated the chemopreventive and therapeutic potential of Carvacrol in several malignancies, including breast cancer, melanoma, hepatocellular carcinoma, cervical cancer, and non-small cell lung cancer
Cyt‑c↑, markedly enhanced cytochrome c expression
FADD↑, . Carvacrol-injected therapy markedly elevated FADD expression
P53↑, Carvacrol receiving rat’s up-regulated P53 concentrations markedly that reached their peak in the injected (## P ≤ 0.01 vs. tumor and **P ≤ 0.01 vs. normal) as well as oral and mixed groups

5894- CAR,    Targeting Gastrointestinal Cancers with Carvacrol: Mechanistic Insights and Therapeutic Potential
- Review, Var, NA
AntiCan↑, Carvacrol has demonstrated strong anticancer properties by modulating multiple molecular pathways governing apoptosis, inflammation, angiogenesis, and metastasis.
Apoptosis↑,
Inflam↓,
angioG↓,
TumMeta↓,
selectivity↑, revealed its ability to selectively target cancer cells while sparing healthy tissue
BioAv↑, nanotechnology have further enhanced its pharmacological profile by improving solubility, stability, and tumor-targeted delivery.
ChemoSen↑, synergistic effects when used in combination with conventional chemotherapeutics.
Dose↝, 84.38% of OEO’s contents are ‘carvacrol’.
TumCP↓, limit metastasis, induce apoptosis, suppress tumor cell proliferation, and improve the effectiveness of traditional chemotherapy medications
hepatoP↑, Carvacrol shows biological activities, such as antimicrobial, antitumor, antimutagenic, antigenotoxic, anti-inflammatory, anti-angiogenic, hepatoprotective, and antihepatotoxic properties.
Casp3↑, induced apoptosis by activating caspase-3 and caspase-9 while downregulating Bcl-2 mRNA levels
Casp9↑,
Bcl-2↓,
ROS↑, carvacrol causes oxidative stress by increasing the production of reactive oxygen species (ROS) and depleting GSH levels, which results in strong lethal effects on AGS gastric cancer
GSH↓,
BAX↑, upregulating pro-apoptotic markers such as Bax, caspase-3, caspase-7, caspase-8, caspase-9, cytochrome C, Fas, Fas-associated death domain (FADD), and p53
Casp7↑,
Casp8↑,
Cyt‑c↑,
Fas↑,
FADD↑,
P53↑,
Bcl-2↓, downregulating anti-apoptotic Bcl-2.
TumMeta↓, preventing metastasis by limiting the migration and invasion of cancer cells by upregulating epithelial markers like E-Cadherin and tissue inhibitors of metalloproteinases 2 and 3 (TIMP2 and TIMP3)
TumCMig↓,
TumCI↓,
E-cadherin↑,
TIMP2↑,
TIMP3↑,
N-cadherin↓, downregulating mesenchymal markers like N-Cadherin and ZEB2
ZEB2↓,
*lipid-P↓, protects the liver from diethylnitrosamine (DEN)-induced hepatocellular carcinogenesis by reducing lipid peroxidation, restoring key liver enzymes (AST, ALT, ALP, LDH, cGT)
*AST↓,
*ALAT↓,
*ALP↓,
*LDH↓,
*SOD↑, and enhancing antioxidant defenses (SOD, CAT, GPx, GR, GSH)
*Catalase↑,
*GPx↑,
*GSR↑,
selectivity↑, while selectively inducing apoptosis in cancer cells without harming normal liver tissue
cl‑PARP↑, inhibits HepG2 cancer cell growth by activating caspase-3, promoting PARP cleavage, downregulating Bcl-2, and modulating the MAPK signaling pathway by selectively reducing ERK1/2 phosphorylation while activating p38
ERK↓,
p38↑,
OS↑, rats (aged 6–8 weeks) demonstrated that carvacrol enhances sorafenib efficacy in HCC, improving survival rates, reducing tumor progression, and mitigating sorafenib-induced cardiac and hepatic toxicity.
AFP↓, carvacrol reduces serum alpha-fetoprotein (AFP) and alpha-L-fucosidase (AFU) levels by downregulating COX-2 and oxidative stress, inhibits angiogenesis via VEGF suppression,
COX2↓,
VEGF↓,
PCNA↓, prevents tumor proliferation by downregulating proliferating cell nuclear antigen (PCNA) and Ki-67 through TNF-α suppression.
Ki-67↓,
TNF-α↓,
BioAv↓, Despite carvacrol’s promising effects in vitro and in vivo, limitations such as bioavailability and solubility challenge its therapeutic application.

6254- CBC/D,    Cynanchum auriculatum Royle ex Wight., Cynanchum bungei Decne. and Cynanchum wilfordii (Maxim.) Hemsl.: Current Research and Prospects
- Review, Var, NA
*neuroP↑, their dry roots as the bioactive part have been revealed to exhibit anti-tumor, neuroprotection, organ protection, reducing liver lipid and blood lipid, immunomodulatory, anti-inflammatory, and other activities
*Imm↑,
*Inflam↓,
CSCs↓, CA at the dosage of 10 mg/kg was demonstrated to inhibit proliferation and formation of breast cancer stem cells
HH↓, CB at the dosage of 50 mg/kg were revealed to block Hedgehog pathway-dependent medulloblastoma by regulating the level of Gli,
Gli↓,
AST↓, CA at the doses of 4 and 8 g/kg were able to decrease the levels of AST and ALT, improve SOD activity, and reduce malondialdehyde content in the in vivo
ALAT↓,
MDA↓,
hepatoP↑, 500 mg/kg was capable of reducing serum ALT and AST levels in mice with hepatic injury induced by CCl4, revealing its feasibility to exert hepatoprotection effect
*NRF2↑, protect them from oxidative toxicity and inflammatory damages by enhancing Nrf2 and HO-1 expression via the NF-κB signaling pathway
*HO-1↑,
NF-kB?, inhibitory protein of NF-κB
GSK‐3β↓, caudatin of CW during the dose of 12.5–50 μM was uncovered to inhibit GSK3β and β-catenin expression, which was attributed to the suppressive effect on wnt protein target genes COX-2, MMP2, and MMP9
β-catenin/ZEB1↓,
COX2↓,
MMP2↑,
MMP9↓,
BioAv↑, suggesting it could be absorbed and distributed rapidly without long-term accumulation in mice tissue

2393- Cela,    Celastrol mitigates inflammation in sepsis by inhibiting the PKM2-dependent Warburg effect
- in-vivo, Sepsis, NA - in-vitro, Nor, RAW264.7
OS↑, Cel protected mice from lethal endotoxemia and improved their survival with sepsis, and it significantly decreased the levels of pro-inflammatory cytokines in mice and macrophages treated with LPS
PKM2↓, Cel bound to Cys424 of pyruvate kinase M2 (PKM2), inhibiting the enzyme and thereby suppressing aerobic glycolysis (Warburg effect).
Glycolysis↓,
Warburg↓,
Inflam↓, Cel inhibits inflammation and the Warburg effect in sepsis via targeting PKM2 and HMGB1 protein.
HMGB1↓, Cel directly binds PKM2 and HMGB1
ALAT↓, pretreatment with Cel followed by LPS significantly reduced serum levels of ALT, AST and urea (
AST↓,
TNF-α↓, Cel pretreatment also decreased the serum levels of TNF-α, IL-1β and IL-6
IL1β↓,
IL6↓,

6660- Cen,    Hepatoprotective effect of Centella asiatica 50% ethanol extract against acetaminophen-induced acute liver injury in BALB/c mice
*hepatoP↑, biomarkers of liver injury, were significantly increased by APAP and dose-dependently decreased by CA-HE50
*NO↓, inhibiting the release of nitric oxide from these cells;
*lipid-P↓, CA-HE50 inhibits lipid peroxidation in the liver
*IL1β↓, xpression of IL-1β was significantly suppressed by all doses of CA-HE50
*ALAT↓, CA-HE50 pre-treatment dose-dependently decreased the APAP-induced increase in levels of serum ALT, AST, and LDH levels, indicating that CA-HE50 has a protective effect against fulminant liver injury.
*AST↓,
*LDH↓,
GSH↑, GSH depletion and MDA overproduction caused by APAP were reversed by CA-HE50 treatment.
MDA↓,

6656- Cen,    Recent insights into therapeutic potential and nanostructured carrier systems of Centella asiatica: An evidence-based review
- Review, Var, NA - Review, AD, NA
AntiCan↑, C. asiatica possesses a broad array of therapeutic effects including anti-ulcer, anti-cancer, anti-diabetic, anti-osteoporotic, neuroprotective, antioxidant, cardioprotective, and anti-inflammatory activities.
*AntiDiabetic↑,
*neuroP↑,
*antiOx↑,
*cardioP↑,
*Inflam↓,
*hepatoP↑, figure 1
*AntiAge↑,
*AST↓,
*ALAT↓,
*LDH↓,
*lipid-P↓,
Casp3↑, anti-cancer fig 1
*memory↑, 1000 mg/kg/d of Centella extract in drinking water improved the deficit's executive function, learning, and recognition memory in aged mice and also attenuated the increased anxiety observed in female mice.
*Wound Healing↑, C. asiatica may accelerate the healing process of wounds by promoting angiogenesis.
eff↑, Fard et al. made silver nanoparticles from C.asiatica leaf extract to study how these nanoparticles kill cancer cells and cause them to commit suicide in the MCF-7 breast cancer cell line.

6650- Cen,    Therapeutic Potential of Centella asiatica and Its Triterpenes: A Review
- Review, AD, NA
*BioAv↝, madecassoside, asiaticoside, madecassic acid, and asiatic acid are widely distributed in the body and madecassoside, asiaticoside may exert their biological activity through converted into aglycone (madecassic acid, and asiatic acid).
*BioAv↝, C. asiatica enhances the function of the nervous system. It dissolves in methanol, ethanol, and water.
*MDA↓, Male Wistar rats – MDA ↓, GSH ↑, SOD ↑, AChE↓
*GSH↑,
*SOD↑,
*AChE↓,
*memory↑, Male SD rats; hippocampal cell – Spatial working memory↑, Ki-67 cells↑
*Ki-67↑,
*Catalase↑, Male SD rats MAPK SOD↑, LPO↑, CAT↑, GSH↑, dopamine↑, glutamate↑, Syn1↑, Stx1A↑, PI3K↑, PDK1↑, PEBP↓, VMAT2↑, TH ↑, MAPK ↑, BDNF↑, NGF↑
*PI3K↑,
*BDNF↑,
*NGF↑,
*ROS↓, Water extract of CA Tg2576 mice – ROS↓, NRF2↑, GCLC↑, HMOX1↑, NQO1↑, ATP↑, Mt-ND1↑, Mt-ATP6↑, Mt-CO1↑, Mt-CYB↑, oxygen consumption rate↑
*NRF2↑,
*HO-1↑,
*NQO1↑,
*ATP↑,
*OCR↑,
*TNF-α↓, Ethanolic extract of CA Male SD rats – TNF-α↓, BDNF↑
*PP2A↑, Ethanolic extract of CA Male albino Wistar rats PP2A/GSK-3B PP2A↑, GSK-3B↓, Bcl-2↑
*GSK‐3β↓,
*Bcl-2↑,
*TrkB↑, Standardized extract of CA Male Wistar rats – NR2A↑, NR2B↑, BDNF↑,TrkB↑
*NOTCH1↑, Asiatic acid Male SD rats – Notch1↑, SOX2↑, DCX↑, Nrf2↑, nestin↑, p21 positive cells↓, MDA↓
*SOX2↑,
*Nestin↑,
*MDA↓,
*MAOA↓, Asiaticoside-D Worms – MAO-A↓, MAO-B↓
*MAOB↓,
*GPx↑, Previous studies found that C. asiatica and its triterpenoids could effectively increase SOD and GPX activities, activate nuclear factor erythroid-2-related factor 2, improve the cognitive impairment of animals,
*cognitive↑,
*ROS↓, C. asiatica and its triterpenoids could reduce ROS production
*neuroP↑, they reduced related nerve cell apoptosis, increased synaptic density, and improved the survival rate of neural cells
*glucose↓, Methanol extract of CA Male SD rats – Blood glucose ↓, food and water intake ↓, ALT↓, AST↓, PFK ↑, GS ↑, GP↑, glycogen content ↑
*ALAT↓,
*AST↓,
*PFK↓,
*Weight↓, inhibit weight gain
*Inflam↓, (4) ameliorate inflammation,
*AntiDiabetic↑, C. asiatica extract and related components (asiatic acid, madecassoside) for the treatment of endocrine diseases such as diabetes, obesity and osteoporosis are excellent.
*Obesity↓,
*Wound Healing↑, The C. asiatica extract and its triterpenoids had certain therapeutic and relieving effects on acne, baldness, vitiligo, atopic dermatitis, and wounds. C. asiatica extract can effectively promote wound healing in diabetic patients
*cardioP↑, C. asiatica has a positive effect on cardiovascular diseases.
*GutMicro↑, C. asiatica and its triterpenoids also have therapeutic effects on digestive disorders, which is mainly reflected by improved liver fibrosis, colitis, and gastric mucosal damage; and even reduced Helicobacter pylori gastric colonization
*Sepsis↓, Asiatic acid can improve the side effects caused by antibiotics, reverse multidrug resistance (MDR), and reduce sepsis.
*BioAv↑, C. asiatica cream containing 5.12% asiaticoside and 5.1% madecassoside can be completely absorbed by the skin and effectively improve pigmentation and may be used in treating hypertrophic scars

2785- CHr,    Emerging cellular and molecular mechanisms underlying anticancer indications of chrysin
- Review, Var, NA
*NF-kB↓, suppressed pro-inflammatory cytokine expression and histamine release, downregulated nuclear factor kappa B (NF-kB), cyclooxygenase 2 (COX-2), and inducible nitric oxide synthase (iNOS)
*COX2↓,
*iNOS↓,
angioG↓, upregulated apoptotic pathways [28], inhibited angiogenesis [29] and metastasis formation
TOP1↓, suppressed DNA topoisomerases [31] and histone deacetylase [32], downregulated tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β)
HDAC↓,
TNF-α↓,
IL1β↓,
cardioP↑, promoted protective signaling pathways in the heart [34], kidney [35] and brain [8], decreased cholesterol level
RenoP↑,
neuroP↑,
LDL↓,
BioAv↑, bioavailability of chrysin in the oral route of administration was appraised to be 0.003–0.02% [55], the maximum plasma concentration—12–64 nM
eff↑, Chrysin alone and potentially in combination with metformin decreased cyclin D1 and hTERT gene expression in the T47D breast cancer cell line
cycD1/CCND1↓,
hTERT/TERT↓,
MMP-10↓, Chrysin pretreatment inhibited MMP-10 and Akt signaling pathways
Akt↓,
STAT3↓, Chrysin declined hypoxic survival, inhibited activation of STAT3, and reduced VEGF expression in hypoxic cancer cells
VEGF↓,
EGFR↓, chrysin to inhibit EGFR was reported in a breast cancer stem cell model [
Snail↓, chrysin downregulated MMP-10, reduced snail, slug, and vimentin expressions increased E-cadherin expression, and inhibited Akt signaling pathway in TNBC cells, proposing that chrysin possessed a reversal activity on EMT
Slug↓,
Vim↓,
E-cadherin↑,
eff↑, Fabrication of chrysin-attached to silver and gold nanoparticles crossbred reduced graphene oxide nanocomposites led to augmentation of the generation of ROS-induced apoptosis in breast cancer
TET1↑, Chrysin induced augmentation in TET1
ROS↑, Pretreatment with chrysin induced ROS formation, and consecutively, inhibited Akt phosphorylation and mTOR.
mTOR↓,
PPARα↓, Chrysin inhibited mRNA expression of PPARα
ER Stress↑, ROS production by chrysin was the critical mediator behind induction of ER stress, leading to JNK phosphorylation, intracellular Ca2+ release, and activation of the mitochondrial apoptosis pathway
Ca+2↑,
ERK↓, reduced protein expression of p-ERK/ERK
MMP↑, Chrysin pretreatment led to an increase in mitochondrial ROS creation, swelling in isolated mitochondria from hepatocytes, collapse in MMP, and release cytochrome c.
Cyt‑c↑,
Casp3↑, Chrysin could elevate caspase-3 activity in the HCC rats group
HK2↓, chrysin declined HK-2 combined with VDAC-1 on mitochondria
NRF2↓, chrysin inhibited the Nrf2 expression and its downstream genes comprising AKR1B10, HO-1, and MRP5 by quenching ERK and PI3K-Akt pathway
HO-1↓,
MMP2↓, Chrysin pretreatment also downregulated MMP2, MMP9, fibronectin, and snail expression
MMP9↓,
Fibronectin↓,
GRP78/BiP↑, chrysin induced GRP78 overexpression, spliced XBP-1, and eIF2-α phosphorylation
XBP-1↓,
p‑eIF2α↑,
*AST↓, Chrysin administration significantly reduced AST, ALT, ALP, LDH and γGT serum activities
ALAT↓,
ALP↓,
LDH↓,
COX2↑, chrysin attenuated COX-2 and NFkB p65 expression, and Bcl-xL and β-arrestin levels
Bcl-xL↓,
IL6↓, Reduction in IL-6 and TNF-α and augmentation in caspases-9 and 3 were observed due to chrysin supplementation.
PGE2↓, Chrysin induced entire suppression NF-kB, COX-2, PG-E2, iNOS as well.
iNOS↓,
DNAdam↑, Chrysin induced apoptosis of cells by causing DNA fragmentation and increasing the proportions of DU145 and PC-3 cells
UPR↑, Also, it induced ER stress via activation of UPR proteins comprising PERK, eIF2α, and GRP78 in DU145 and PC-3 cells.
Hif1a↓, Chrysin increased the ubiquitination and degradation of HIF-1α by increasing its prolyl hydroxylation
EMT↓, chrysin was effective in HeLa cell by inhibiting EMT and CSLC properties, NF-κBp65, and Twist1 expression
Twist↓,
lipid-P↑, Chrysin disrupted intracellular homeostasis by altering MMP, cytosolic Ca (2+) levels, ROS generation, and lipid peroxidation, which plays a role in the death of choriocarcinoma cells.
CLDN1↓, Chrysin decreased CLDN1 and CLDN11 expression in human lung SCC
PDK1↓, Chrysin alleviated p-Akt and inhibited PDK1 and Akt
IL10↓, Chrysin inhibited cytokines release, TNF-α, IL-1β, IL-10, and IL-6 induced by Ni in A549 cells.
TLR4↓, Chrysin suppressed TLR4 and Myd88 mRNA and protein expression.
NOTCH1↑, Chrysin inhibited tumor growth in ATC both in vitro and in vivo through inducing Notch1
PARP↑, Pretreating cells with chrysin increased cleaved PARP, cleaved caspase-3, and declined cyclin D1, Mcl-1, and XIAP.
Mcl-1↓,
XIAP↓,

6299- Cro,    Protective Effects of Crocetin on Arsenic Trioxide-Induced Hepatic Injury: Involvement of Suppression in Oxidative Stress and Inflammation Through Activation of Nrf2 Signaling Pathway in Rats
- in-vivo, Nor, NA
*ALAT↓, Crocetin significantly inhibited ATO-induced alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) increases.
*AST↓,
*ALP↓,
*MDA↓, Crocetin prevented ATO-induced liver malondialdehyde (MDA) and reactive oxygen species (ROS) levels.
*ROS↓, Crocetin reduces the level of ROS induced by ATO.
*Catalase↑, Crocetin abrogated the ATO-induced decrease of catalase (CAT) and superoxide dismutase (SOD) activity.
*SOD↑,
*IL6↓, significantly restore the protein levels of interleukin 6 (IL-6), interleukin 1β (IL-1β), and tumor necrosis factor-alpha (TNF-α).
*IL1β↓, Results indicate that IL-6, IL-1β, and TNF-α were dramatically elevated in the ATO treated group compared with the control group. CRO, meanwhile, was found to markedly restore the protein levels of IL-6, IL-1β, and TNF-α to normal levels
*TNF-α↓,
*NRF2↑, crocetin promoted the expression of nuclear factor erythroid 2 related factor 2 (Nrf2), heme oxygenase-1 (HO-1), and NADP(H): quinone oxidoreductase 1 (NQO1).
*HO-1↑,
*NADPH↑,
*NQO1↑,
*hepatoP↑, These findings suggest that crocetin ameliorates ATO-induced hepatic injury in rats.
*GSH↑, crocetin was found to up-regulate the generation of SOD, CAT, and GSH (which are suppressed by ATO).

6529- CRV,    D-Carvone Attenuates CCl4-Induced Liver Fibrosis in Rats by Inhibiting Oxidative Stress and TGF-ß 1/SMAD3 Signaling Pathway
- in-vivo, Nor, NA
*ALAT↓, D-carvone significantly enhanced liver functions (ALT, AST), oxidant/antioxidant status (MDA, SOD, GSH, total antioxidant capacity; TAC), as well as histopathological changes.
*AST↓, administration with D-carvone (50 mg/kg, bw) significantly reduced serum ALT and AST to 54.8% and 51% compared to the CCl4 model group, respectively
*MDA↓, decreased the MDA levels to 50.7%, while it restored the depleted GSH and SOD levels to 233% and 221.5%, respectively
*SOD↑,
*GSH↑,
*TAC↑,
*eff↑, D-carvone effectively attenuated the progression of liver fibrosis, evident by the decreased collagen deposition and fibrosis score by Masson trichrome staining (MT) and α-SMA protein expression
*TGF-β1↓, significant downregulation of the pro-fibrogenic markers TGF-β1 and SMAD3 and upregulation of MMP9.
*SMAD3↓,
*MMP9↑,
*NRF2↑, D-carvone promotes the Nrf2 signaling pathway which might contribute to the antioxidative activity of D-carvone
*antiOx↑,
*hepatoP↑,
*Inflam↓, D-carvone administration appreciably reduced the inflammatory cells’ infiltration and pro-inflammatory modulators release provoked by liver injury
*NF-kB↓, D-carvone include downregulation of NF-κB
*NO↓, D-carvone has been reported to diminish the excessively produced NO by macrophages and Kupffer cells in the injured liver
*cAMP↑, carvone has been found to activate the cyclic adenosine monophosphate (cAMP) signaling pathway
*ROS↓, by Inhibiting Oxidative Stress

2819- CUR,  Chemo,    Curcumin as a hepatoprotective agent against chemotherapy-induced liver injury
- Review, Var, NA
*hepatoP↑, Several studies have shown that curcumin could prevent and/or palliate chemotherapy-induced liver injury
*Inflam↓, mainly due to its anti-inflammatory, antioxidant, antifibrotic and hypolipidemic properties.
*antiOx↑,
*lipid-P↓, Curcumin can lower lipid peroxidation by increasing the content of GSH, a major endogenous antioxidant,
*GSH↑,
*SOD↑, as well as by enhancing the activity of endogenous antioxidant enzymes, such as SOD, CAT, GPx and GST
*Catalase↑,
*GPx↑,
*GSTs↑,
*ROS↓, elimination of ROS
*ALAT↓, attenuated the increase in serum levels of TNF-α as well as several liver enzymes, including ALT, AST, alkaline phosphatase and MDA which are markers of liver damage caused by MTX or cisplatin.
*AST↓,
*MDA↓,
*NRF2↑, Curcumin also attenuated DILI through activation of the nuclear factor-erythroid 2-related factor 2 (Nrf2) signaling pathway
*COX2↑, Curcumin can also inhibit the expression of cyclooxygenase-2 (COX-2)
*NF-kB↓, NF-κB inhibition, which decreased the downstream induction of COX-2, ICAM-1 and MCP-1 pro-inflammatory regulators
*ICAM-1↓,
*MCP1↓,
*HO-1↑, increase in HO-1 and NQO1 expression
CXCc↓, Downregulation of pro-inflammatory chemokines, (CXCL1, CXCL2, and MCP-1)

6715- dietF,    Are Fermented Foods Effective against Inflammatory Diseases?
- Review, Nor, NA
*Imm↑, Fermented foods containing probiotic bacteria and fungi can enhance the immune system, improve gastrointestinal health, and lower the risk of developing various inflammatory diseases.
*GastroP↑,
*Inflam↓,
AntiCan↑, Kombucha tea possesses anticancer, antimicrobial, and hepatoprotective properties
*AntiBio↑,
*hepatoP↑,
*CD4+↑, Kombucha consumption also reduced inflammation by increasing polarization of CD4+ T cells (by induction of IL-4 and TGF-β) and by inhibiting IFN-γ and IL-17
*IFN-γ↓,
*IL17↓,
*GutMicro↑, Kombucha intake also promoted the growth of butyrate-producing bacteria in the gut that exert anti-inflammatory effects
*antiOx↑, fermented turmeric demonstrated stronger antioxidative activity than raw turmeric.
*AST↓, After 5 days of fermentation with Bacillus natto, fermented turmeric dramatically decreased the levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in contrast to unfermented turmeric.
*ALAT↓,
*HDL↑, After fermentation, there was a considerable rise in HDL cholesterol and a significant decrease in LDL cholesterol [45].
*LDL↓,
*ROS↓, Kimchi has also demonstrated potent radical scavenging and antioxidant activity in vitro, enhancing LLC-PK1 cell viability by protection against lipid peroxidation.
*lipid-P↓,
*Inflam↓, The anti-inflammatory properties of sauerkraut LAB were emphasized in a randomized, double-blinded pilot study on 34 Norwegian inflammatory bowel syndrome (IBS) patients.
*Aβ↓, Mice fed with doenjang-infused high-fat feed had reduced β-amyloid peptide (Aβ) and neuroinflammatory gene levels, further reinforcing the protective effect of fermented soy on the aging brain

3707- dietSTF,    Intermittent fasting protects against the deterioration of cognitive function, energy metabolism and dyslipidemia in Alzheimer’s disease-induced estrogen deficient rats
- in-vivo, AD, NA
*memory↑, Intermittent fasting also prevented memory loss: short-term and special memory loss.
*Aβ↓, the rats in the AD-IMF groups exhibited less β-amyloid deposition than those in the AD-AL
*AST↓, Serum aspartate transaminase (AST) and alanine transaminase (ALT) levels, indexes of liver damage, were not significantly changed by AD but they were greatly lowered by IMF.
*ALAT↓,

6347- DRE,    Protective Effects of Taraxacum officinale L. (Dandelion) Root Extract in Experimental Acute on Chronic Liver Failure
*hepatoP↑, reduced serum liver injury markers (AST, ALT, ALP, GGT, total bilirubin), renal tests (creatinine, urea), and oxidative stress tests (TOS, OSI, MDA, NO, 3NT).
*AST↓,
*ALAT↓,
*ALP↓,
*Bil↓,
*creat↓,
*TOS↑,

6357- DRE,    New Perspectives on the Effect of Dandelion, Its Food Products and Other Preparations on the Cardiovascular System and Its Diseases
- Review, Nor, NA
*cardioP↑, describes the cardioprotective potential of dandelion products and preparations.
*Dose↝, Dandelion is a rich source of phenolic acids (chicoric acid, chlorogenic acid), flavonoids (luteolin derivatives, quercetin), and terpenes (sesquiterpene lactones).
*Dose↝, It is also a strong source of vitamins (A, C, E, K, and B) and minerals (calcium, sodium, magnesium, iron, copper, silicon, zinc, manganese)
*toxicity∅, Although dandelion is mainly known for its medicinal properties, it has for many years been successfully used worldwide in the food industry as an entirely non-toxic and edible plant
*toxicity↓, dose should not exceed 4 g or 12 g per day for the aerial parts of the plant or 1 g or 3 g per day for the root. The roots, leaves, and flowers may be eaten raw or cooked
*BP↓, Dandelion leaves are also believed to have a positive effect on the cardiovascular system due to their high potassium content (397 mg potassium/100 g): increased potassium intake with food (about 3500 mg/day for an adult) has been found to lower BP
*Inflam↓, sesquiterpene lactones, which have been found to have anti-inflammatory and antibacterial effects, as well as triterpenes or phytosterols, which possess anti-atherosclerotic properties
*Bacteria↓,
*Imm↑, roots are also rich in inulin, which has a probiotic, hypoglycemic, and immune-boosting effect
*lipid-P↓, extract was found to elevate total antioxidant capacity and decrease lipid peroxidation, a marker of oxidative stress, in the heart, liver, kidney, and brain, among others.
*AST↓, ; treatment was found to improve the lipid profile and aspartate aminotransferase (AST) and alanine aminotransferase (ALT) concentrations in obese mice.
*ALAT↓,
*AntiAg↑, extracts E2 and E3 and fractions A, B, and C significantly inhibited ADP-activated platelet adhesion to fibrinogen, while flavonoid fractions A to C inhibited thrombin-activated platelet adhesion at both tested doses (10 and 50 μg/mL)
*ROS↓, (1) the inhibition of reactive oxygen species (ROS) production;
*AntiThr↑, antithrombotic effects.

1607- EA,    Exploring the Potential of Ellagic Acid in Gastrointestinal Cancer Prevention: Recent Advances and Future Directions
- Review, GC, NA
STAT3↓, EA inhibits STAT3 signaling
TumCP↓, EA inhibits cell proliferation, induces apoptosis
Apoptosis↑,
NF-kB↓, inhibiting nuclear factor-kappa B
EMT↓, suppressing epithelial–mesenchymal transition
RadioS↑, In liver cancer, EA exhibits radio-sensitizing effects
antiOx↑, As a potential antioxidant agent,
COX1↓, EA suppresses the expression of several factors, including COX1, COX2, c-myc, snail, and twist1
COX2↓,
cMyc↓,
Snail↓,
Twist↓,
MMP2↓, significantly decreased MMP-2 and MMP-9 expression and activity.
P90RSK↓,
CDK8↓, downregulate CDK8 expression and activity
PI3K↓, inactivating PI3K/Akt signaling
Akt↓,
TumCCA↑, promote cell cycle arrest
Casp8↑, ctivating caspase-8, and lowering proliferating cell nuclear antigen (PCNA) expression,
PCNA↓,
TGF-β↓,
Shh↓, suppression of the Akt, Shh, and Notch pathways, EA can prevent the growth, angiogenesis, and metastasis of pancreatic cancer
NOTCH↓,
IL6↓,
ALAT↓, decreasing liver injury biomarkers such as alanine transaminase (ALT), alkaline phosphatase (ALP), and aspartate aminotransferase (AST)
ALP↓,
AST↓,
VEGF↓,
P21↑,
*toxicity∅, no toxicity was found for a 50% effective dose by the intraperitoneal route inferior to 1 mg/kg/day
*Inflam↓, ncluding anti-inflammatory [10], anti-oxidant [11], anti-allergic [12], and anti-mutagenic [13] properties, as well as potential health advantages like gastroprotective [14], cardioprotective [15], neuroprotective [16, 17], and hepatoprotective [18,
*cardioP↑,
*neuroP↑,
*hepatoP↑,
ROS↑, Exposure to EAs induced apoptosis, accelerated cell cycle arrest, and elevated the generation of reactive oxygen intermediates [59].
*NRF2↓, As a potential antioxidant agent, it scavenges reactive oxygen species (ROS), and by upregulating of Nrf2,
*GSH↑, Moreover, EA increases reduced glutathione (GSH), which is critical for cellular defense against oxidative stress and liver damage,

6819- EMD,    Recent advances in the therapeutic potential of emodin for human health
- Review, Nor, NA
AntiCan↑, It has therapeutic effects in cancer, diabetes, neurodegenerative diseases or chronic inflammatory diseases.
*AntiDiabetic↑, anticancer, neuroprotective, antidiabetic, antioxidant and anti-inflammatory.
*neuroP↑,
*Inflam↓,
*antiOx↑,
*BioAv↓, Because its bioavailability is low, there are limitations in clinical therapeutic use.
*BioAv↑, combined administration of emodin and piperine has been observed to clinically improve emodin pharmacokinetics, increasing 221 % of the area under the curve (AUC), 258 % the maximum concentration (Cmax), and decreasing 230 % the clearance related to
*SOD↑, fig 2 antioxidant
*GPx↑,
*GSH↑,
*NRF2↑,
*ROS↓,
*lipid-P↓,
*Cyt‑c↓,
*BAX↓, fig 2 antiinflammatory
*Bcl-2↓,
*iNOS↓,
*NO↓,
*IL6↓,
*IL10↓,
*IL17↓,
*IFN-γ↓,
*NF-kB↓,
*LC3II↓,
*Akt↓,
*Beclin-1↓,
*AMPK↓, fig 2 neuroprotective
*TNF-α↓,
*PGE2↓,
*Apoptosis↓,
*Casp3↓,
*Casp9↓,
*P53↓,
*P21↓,
*NAD↓, neuronal oxidative stress
*ATP↓,
*CHOP↓,
*GADD34↓,
*ATF4↓,
tumCV↓, fig 2 anticancer
Apoptosis↑,
TumCG↓,
TumCI↓,
TumMeta↓,
CSCs↓, glioma stem cells ↓b-catenin, ↓Notch-1, ↓STAT3
NOTCH1↓,
STAT3↓,
eff↑, emodin combined with curcumin ↓proliferation, ↑miR-34a
miR-34a↓,
*neuroP↑, Neuroprotective LPS-stimulated mouse ↓Nrf-2, NQO1, ↓TNF-α,↓↓ IL-6, ↓NO, ↓PGE2
*BDNF↓, model of chronic stress mice in vivo ↓progression of behavioral impairments in mice ↓consumption of sucrose, ↓plasmatic corticosterone, ↓mRNA, ↓BDNF,
*hepatoP↑, Hepatoprotective rats in vivo ↓ethanol-mediated liver steatosis ↓ ALT, ↓AST, ↓ TGL
*ALAT↓,
*AST↓,
TG/TAG↓,
ROS↑, However, at higher concentrations, emodin significantly increased ROS generation and reduced cell viability.
Slug↓, expression levels of Slug (a transcription factor) were also suppressed with emodin treatment.
EMT↓, results suggested that emodin suppressed the epithelial-mesenchymal transition of cancer cells through the ILK/GSK-3β/Slug signaling pathway
Glycolysis↓, In addition, emodin inhibited glycolysis via ROS-induced inactivation of the PI3K/AKT signaling pathway.
ChemoSen↑, The study by Peng et al. [130] also showed chemosensitizing effects of emodin to cisplatin in A549 (2–20 µM, for 48 h) and H460 (0.5–10 µM) non-small cell lung cancer cells.
P-gp↓, The sensitization mechanism was mediated by the inhibition of P-glycoprotein (Pgp), a drug-resistant protein related to the efflux pump mechanism.
Ki-67↓, The significant reduction of Ki-67 and proliferating cell nuclear antigen (PCNA) protein levels supported the antiproliferative effect of emodin in animal models.
PCNA↓,
ER Stress↑, findings suggested that emodin exerts its apoptotic effects in a process mediated by ER stress and the activation of the TRIB3/NF-κB pathway in lung cancer cells.
TRIB3↑,
NF-kB↑,
TumMeta↑, Emodin (40 mg/kg for 7 days) significantly decreased the metastatic recurrence of breast cancer after surgery in the lungs by reducing the formation of epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC).
*Imm↓, emodin may be developed as an immunosuppressive agent in case of immune activation, autoimmune disorders even in organ transplantation
*toxicity↝, An excess of emodin due to its laxative effects causes intestinal pain and severe diarrhea with subsequent electrolyte imbalance and dehydration [157]. Therefore, treatment should begin when symptoms appear, with special attention to electrolyte leve

6825- EMD,    Advances in the pharmacological effects and molecular mechanisms of emodin in the treatment of metabolic diseases
- Review, Nor, NA
*Inflam↓, Emodin has a variety of pharmacological effects, including anti-inflammatory, anti-tumor, antibacterial, immune enhancement, lipid-lowering, blood glucose-lowering, kidney protection, etc.
*AntiTum↑,
*Bacteria↓,
*Imm↑,
*glucose↓,
*RenoP↑,
*TLR4↓, i.p 40 mg/kg Inactivating the TLR4/MyD88/NF-κB/NLRP3 pathway
*MyD88↓,
*NLRP3↓,
*NF-kB↓, 20 μM Inhibiting ROS-mediated NF-κB activation
*PI3K↓, Inhibiting the PI3K/mTOR/GSK3β signaling pathway
*mTOR↓,
*GSK‐3β↓,
*Hif1a↓, LPS-induced acute lung injury (ALI) in rats oral 20 mg/kg, 40 mg/kg Inhibiting the mTOR/HIF-1α/VEGF signaling pathway
*VEGF↓,
*GutMicro↑, oral 8.75, 17.5 and 35 mg/kg Increasing the abundance of beneficial intestinal microbiota and inhibiting the abundance of harmful bacteria
*Obesity↓, Similarly, in high-fat diet-induced obese mice, treatment with emodin (80 mg/kg) reduced body weight
*AntiDiabetic↑, emodin also has a good therapeutic effect on diabetic neuropathic pain (DNP), diabetic cardiomyopathy (DCM), and diabetic gastroenteropathy.
*AMPK↑, Emodin upregulates AMPK phosphorylation, downregulates mTOR phosphorylation, and reduces the expression of Bcl-2-associated X protein (Bax) and cysteine-dependent aspartate-specific proteases-3 (caspase-3), indicating that emodin actively regulates a
*PPARγ↑, Most current research results indicate that emodin has the effect of activating PPARγ in a dose-dependent manner
*PPARγ↓, however, the research results of Yang et al. showed that emodin can reduce the expression of PPARγ and enhance the expression of Runx2 and OSX, thereby enhancing the differentiation into osteoblasts
*toxicity↝, Although emodin has shown hepatoprotective effects in many studies, Zheng et al. showed hepatotoxicity when a large concentration of emodin (160 μM) was administered to L02 cells,
*hepatoP↑, whereas hepatoprotective effects were observed when emodin concentrations were controlled at 10–80 μM
*AST↓, the liver function test results showed that emodin at doses of 40 mg/kg and 80 mg/kg had a better effect on reducing AST and ALT than 160 mg/kg
*ALAT↓,

6827- EMD,    Mechanism of Emodin in the Treatment of Rheumatoid Arthritis
- Review, Arthritis, NA
*ALAT↓, emodin can improve ethanol-mediated hepatic steatosis and treat alcoholic liver disease by downregulating the levels of alanine aminotransferase (ALT), triglyceride, and aspartate aminotransferase
*AST↓,
*ROS↓, emodin exerts potential antioxidant effects, such as regulating the free radical and reactive oxygen species (ROS) levels and affecting oxidative stress-induced damage
*cardioP↑, In cardiovascular diseases, emodin exerts potential therapeutic effects on diabetic retinopathy by inhibiting aldose reductase activity and improving retinal angiogenesis
*TNF-α↓, Emodin can also significantly inhibit the expression of TNF-α and activate the NF-κB signaling pathway in the local myocardial infarction area and can play a protective role in myocardial ischemia
*NF-kB↓,
*Inflam↓, Emodin Affects RA Procession by Regulating Inflammatory Cytokines
*AntiArt↑,
*PGE2↓, PGE2, MMP-3, MMP-13, ADAMTS-4, and ADAMTS-5 decreased expression
*MMP3↓,
*MMP13↓,
*COX2↓, Emodin also reduces the plasma levels of TNF-α and IL-6, PGE(2) production, and cyclooxygenase 2 (COX-2) protein expression in synovial tissue [102].
*AntiCan↑, Emodin is a natural anthraquinone compound with various pharmacological effects, including anticancer, anti-inflammatory, antiviral, antibacterial, antiallergic, antiosteoporosis, antidiabetic, immunosuppressive, neuroprotective, and hepatoprotective
*neuroP↑,
*hepatoP↑,

6385- Eug,    Anticancer potential of eugenol in hepatocellular carcinoma through modulation of oxidative stress, inflammation, apoptosis, and proliferation mechanisms
- in-vivo, HCC, HepG2
tumCV↓, eugenol reduced cell viability (IC50 of 189.29 µg/mL) and inhibited cell migration in the HCC cell line HepG2.
TumCMig↓,
*ALAT↓, Eugenol treatment significantly reduced the activity levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP), along with the levels of total bilirubin (TBIL), alpha-fetoprotein (AFP),
*AST↓,
*ALP↓,
*Bil↓,
*CEA↓, carcinoembryonic antigen (CEA), carbohydrate antigen 19–9 (CA 19–9), lipid peroxides (LPO), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β).
*lipid-P↓,
*TNF-α↓,
*IL1β↓,
NF-kB↓, (NF-κB), interleukin-8, C-X-C Motif Chemokine Receptor 3 (CXCR3), B-cell lymphoma 2 (Bcl-2), IQ Motif Containing GTPase Activating Protein 1 (IQGAP1), IQ Motif Containing GTPase Activating Protein 3 (IQGAP3), Harvey rat sarcoma viral oncogene homolo
CXCR3↓,
HRAS↓, Harvey rat sarcoma viral oncogene homolog (HRAS), Kirsten rat sarcoma viral oncogene homolog (KRAS), and Ki-67 were downregulated following eugenol
KRAS↓,
Ki-67↓,
*GSH↑, eugenol supplementation significantly enhanced glutathione (GSH) content, as well as the activities of glutathione peroxidase (GPx) and superoxide dismutase (SOD), and the levels of nuclear factor erythroid 2-related factor 2 (Nrf2).
*GPx↑,
*SOD↑,
*NRF2↑,
P53↑, expressions of tumor suppressor gene p53, Bcl-2-associated X protein (BAX), death receptor 4 (DR4), death receptor 5 (DR5), decoy receptor 1 (DcR1), programmed cell death 5 (PDCD5), and IQ Motif Containing GTPase Activating Protein 2 (IQGAP2) were ma
BAX↑,
DR4↑,
DR5↑,

1656- FA,    Ferulic Acid: A Natural Phenol That Inhibits Neoplastic Events through Modulation of Oncogenic Signaling
- Review, Var, NA
tyrosinase↓,
CK2↓,
TumCP↓,
TumCMig↓,
FGF↓,
FGFR1↓,
PI3K↓,
Akt↓,
VEGF↓,
FGFR1↓,
FGFR2↓,
PDGF↓,
ALAT↓,
AST↓,
TumCCA↑, G0/G1 phase arrest
CDK2↓,
CDK4↓,
CDK6↓,
BAX↓,
Bcl-2↓,
MMP2↓,
MMP9↓,
P53↑,
PARP↑,
PUMA↑,
NOXA↑,
Casp3↑,
Casp9↑,
TIMP1↑,
lipid-P↑,
mtDam↑,
EMT↓,
Vim↓,
E-cadherin↓,
p‑STAT3↓,
COX2↓,
CDC25↓,
RadioS↑,
ROS↑,
DNAdam↑,
γH2AX↑,
PTEN↑,
LC3II↓,
Beclin-1↓,
SOD↓,
Catalase↓,
GPx↓,
Fas↑,
*BioAv↓, ferulic acid stability and limited solubility in aqueous media continue to be key obstacles to its bioavailability, preclinical efficacy, and clinical use.
cMyc↓,
Beclin-1↑, ferulic acid by elevating the levels of the apoptosis and autophagy biomarkers, including beclin-1, Light chain (LC3-I/LC3-II), PTEN-induced putative kinase 1 (PINK-1), and Parkin
LC3‑Ⅱ/LC3‑Ⅰ↓,

4022- FulvicA,  Chemo,    Shilajit potentiates the effect of chemotherapeutic drugs and mitigates metastasis induced liver and kidney damages in osteosarcoma rats
- in-vivo, OS, NA
AST↓, Co-treatment of shilajit and drug cocktails also markedly alleviated histopathological changes in liver and kidney tissues.
ALAT↓, (AST)* and alanine aminotransferase (ALT), alkaline phosphatase (ALP), total proteins, albumin, bilirubin, creatinine, urea, and uric acid.
ALP↓,
Bil↝,
creat↓,
uricA↓,
ChemoSen↑, shilajit may potentiate the effects of chemotherapy drugs and mitigate the metastasis-induced liver and kidney damage in osteosarcoma.
chemoP↑,

2525- H2,    Hydrogen-Rich Saline Attenuates Cardiac and Hepatic Injury in Doxorubicin Rat Model by Inhibiting Inflammation and Apoptosis
- in-vivo, NA, NA
OS↓, intraperitoneal injection of hydrogen-rich saline (H2 saline) ameliorated the mortality, cardiac dysfunction, and histopathological changes caused by DOX in rats
cardioP↑,
*AST↓, serum brain natriuretic peptide (BNP), aspartate transaminase (AST), alanine transaminase (ALT), albumin (ALB), tissue reactive oxygen species (ROS), and malondialdehyde (MDA) levels were also attenuated after H2 saline treatment.
ALAT↓,
*ROS↓,
*MDA↓,
*hepatoP↑, H2 saline treatment could inhibit cardiac and hepatic inflammation
*Inflam↓,
chemoP↑, protective effect of H2 saline on DOX-induced cardiotoxicity and hepatotoxicity in rats by inhibiting inflammation and apoptosis.

2524- H2,    Protective effect of hydrogen-rich water on liver function of colorectal cancer patients treated with mFOLFOX6 chemotherapy
- Trial, NA, NA
hepatoP↑, protective effect of hydrogen-rich water on the liver function of colorectal cancer (CRC) patients treated with mFOLFOX6 chemotherapy.
ALAT↓, The hydrogen-rich water group exhibited no significant differences in liver function before and after treatment, whereas the placebo group exhibited significantly elevated levels of ALT, AST and IBIL
AST↓,
Dose↝, Hydrogen-rich water was prepared by increasing the hydrogen pressure in the solution (7). First, the partial air pressure in the water was reduced using a 1406 type vacuum pump
Dose↝, started drinking hydrogen-rich water 1 day prior to chemotherapy until the end of the cycle, for a total of 4 days, with a daily intake of 1,000 ml in 4 doses (250 ml each). Hydrogen-rich water was consumed 0.5 h after a meal and before bedtime.

2868- HNK,    Honokiol: A review of its pharmacological potential and therapeutic insights
- Review, Var, NA - Review, Sepsis, NA
*P-gp↓, reduction in the expression of defective proteins like P-glycoproteins, inhibition of oxidative stress, suppression of pro-inflammatory cytokines (TNF-α, IL-10 and IL-6),
*ROS↓,
*TNF-α↓,
*IL10↓,
*IL6↓,
eIF2α↑, Bcl-2, phosphorylated eIF2α, CHOP,GRP78, Bax, cleaved caspase-9 and phosphorylated PERK
CHOP↑,
GRP78/BiP↑,
BAX↑,
cl‑Casp9↑,
p‑PERK↑,
ER Stress↑, endoplasmic reticulum stress and proteins in apoptosis in 95-D and A549 cells
Apoptosis↑,
MMPs↓, decrease in levels of matrix metal-mloproteinases, P-glycoprotein expression, the formation of mammosphere, H3K27 methyltransferase, c-FLIP, level of CXCR4 receptor,pluripotency-factors, Twist-1, class I histone deacetylases, steroid receptor co
cFLIP↓,
CXCR4↓,
Twist↓,
HDAC↓,
BMPs↑, enhancement in Bax protein, and (BMP7), as well as interference with an activator of transcription 3 (STAT3), (mTOR), (EGFR), (NF-kB) and Shh
p‑STAT3↓, secreased the phosphorylation of STAT3
mTOR↓,
EGFR↓,
NF-kB↓,
Shh↓,
VEGF↓, induce apoptosis, and regulate the vascular endothelial growth factor-A expression (VEGF-A)
tumCV↓, human glioma cell lines (U251 and U-87 MG) through inhibition of colony formation, glioma cell viability, cell migration, invasion, suppression of ERK and AKT signalling cascades, apoptosis induction, and reduction of Bcl-2 expression.
TumCMig↓,
TumCI↓,
ERK↓,
Akt↓,
Bcl-2↓,
Nestin↓, increased the Bax expression, lowered the CD133, EGFR, and Nesti
CD133↓,
p‑cMET↑, HKL through the downregulating the phosphorylation of c-Met phosphorylation and stimulation of Ras,
RAS↑,
chemoP↑, Cheng and coworker determined the chemopreventive role of HKL against the proliferation of renal cell carcinoma (RCC) 786‑0 cells through multiple mechanism
*NRF2↑, , HKL also effectively activate the Nrf2/ARE pathway and reverse this pancreatic dysfunction in in vivo and in vitro model
*NADPH↓, (HUVECs) such as inhibition of NADPH oxidase activity, suppression of p22 (phox) protein expression, Rac-1 phosphorylation, reactive oxygen species production, inhibition of degradation of Ikappa-B-alpha, and suppression of activity of of NF-kB
*p‑Rac1↓,
*ROS↓,
*IKKα↑,
*NF-kB↓,
*COX2↓, Furthermore, HKL treatment the inhibited cyclooxygenase (COX-2) upregulation, reduces prostaglandin E2 production, enhanced caspase-3 activity reduction
*PGE2↓,
*Casp3↓,
*hepatoP↑, compound also displayed hepatoprotective action against oxidative injury in tert-butyl hydroperoxide (t-BHP)-injured AML12 liver cells in in vitro model
*antiOx↑, compound reduces the level of acetylation on SOD2 to stimulate its antioxidative action, which results in reduced reactive oxygen species aggregation in AML12 cells
*GSH↑, HKL prevents oxidative damage induced by H2O2 via elevating antioxidant enzymes levels which includes glutathione and catalase and promotes translocation and activation transcription factor Nrf2
*Catalase↑,
*RenoP↑, imilarly, the compound protects renal reperfusion/i-schemia injury (IRI) in adult male albino Wistar rats via reducing theactivities of serum alkaline phosphatase (ALP), aspartate aminotrans- ferase (AST) and alanine aminotransferase (ALT)
*ALP↓,
*AST↓,
*ALAT↓,
*neuroP↑, Several reports and works have shown that HKL displays some neuroprotective properties
*cardioP↑, Cardioprotection
*HO-1↑, the expression level of heme oxygenase-1 (HO-1)was remarkably up-regulated and miR-218-5p was significantly down-regulated in septic mice treated with HKL
*Inflam↓, anti-inflammatory action of HKL at dose of 10 mg/kg in the muscle layer of mice

4238- HNK,    Neuropharmacological potential of honokiol and its derivatives from Chinese herb Magnolia species: understandings from therapeutic viewpoint
- Review, AD, NA - NA, Park, NA
*BDNF↑, honokiol treatment led to an improvement in plasma BDNF levels.
*hepatoP↑, prevented liver damage by reducing transaminase levels (ALT and AST), liver OS, and TNF-α activity in mice challenged with LPS.
*ALAT↓,
*AST↓,
*TNF-α↓,
*SIRT3↑, 0.5, 1, 2, 5, 10 and 20 μM Enhanced SIRT3 expression, reduced Aβ levels
*Aβ↓,
*Apoptosis↓, Honokiol exhibited a dose-dependent reduction in hippocampal neural apoptosis, ROS generation, and decline in the membrane potential of mitochondria caused by AβO
*ROS↓,
*MMP↑,
*Ca+2↓, Dose-dependent reduction of ROS, suppression of intracellular Ca elevation, and inhibition of caspase-3 activity
*Casp3↓,
*Ach↑, Increased extracellular acetylcholine release to 165.5 ± 5.78% of the basal level
*PPARγ↑, Increased the expression of PPARγ and PGC1α
*PGC-1α↑,
*motorD↑, Improvement of motor dysfunction due to reversal of nigrostriatal dopaminergic neuronal loss
*TNF-α↓, Attenuated the levels of ROS, TNF-α, and IL-1β in both the in vivo and in vitro
*IL1β↓,

2921- LT,    Luteolin as a potential hepatoprotective drug: Molecular mechanisms and treatment strategies
- Review, Nor, NA
*hepatoP↑, Due to its excellent liver protective effect, luteolin is an attractive molecule for the development of highly promising liver protective drugs.
*AMPK↑, fig2
*SIRT1↑,
*ROS↓,
STAT3↓,
TNF-α↓,
NF-kB↓,
*IL2↓,
*IFN-γ↓,
*GSH↑,
*SREBP1↓,
*ZO-1↑,
*TLR4↓,
BAX↑, anti cancer
Bcl-2↓,
XIAP↓,
Fas↑,
Casp8↑,
Beclin-1↑,
*TXNIP↓, luteolin inhibited TXNIP, caspase-1, interleukin-1β (IL-1β) and IL-18 to prevent the activation of NLRP3 inflammasome, thereby alleviating liver injury.
*Casp1↓,
*IL1β↓,
*IL18↓,
*NLRP3↓,
*MDA↓, inhibiting oxidative stress and regulating the level of malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione (GSH)
*SOD↑,
*NRF2↑, luteolin promoted the activation of the Nrf2/ antioxidant response element (ARE) pathway and NF-κB cell apoptosis pathway, thereby reversing the decrease in Nrf2 levels(lead induced liver injury)
*ER Stress↓, down regulate the formation of nitrotyrosine (NT) and endoplasmic reticulum (ER) stress induced by acetaminophen, and alleviate liver injury
*ALAT↓, ↓ALT, AST, MDA, iNOS, NLRP3 ↑GSH, SOD, Nrf2
*AST↓,
*iNOS↓,
*IL6↓, ↓TXNIP, NLRP3, TNF-α, IL-6 ↑HO-1, NQO1
*HO-1↑,
*NQO1↑,
*PPARα↑, ↓TNF-α, IL-6 IL-1β, Bax ↑PPARα
*ATF4↓, ↓ALT, AST, TNF-α, IL-6, MDA, ATF-4, CHOP ↑GSH, SOD
*CHOP↓,
*Inflam↓, Luteolin ameliorates MAFLD through anti-inflammatory and antioxidant effects
*antiOx↑,
*GutMicro↑, luteolin could significantly enrich more than 10% of intestinal bacterial species, thereby increasing the abundance of ZO-1, down regulating intestinal permeability and plasma lipopolysaccharide

3268- Lyco,    Lycopene as a Natural Antioxidant Used to Prevent Human Health Disorders
- Review, AD, NA
*BioAv↓, Lycopene bioavailability can be decreased by ageing, and some of the pathological states, such as cardiovascular diseases (CVDs)
*AntiCan↑, For instance, it has been shown that a higher dietary intake and circulating concentration of lycopene have protective effects against prostate cancer (PCa), in a dose-dependent way
*ROCK1↓, It remarkably lessened the expression of ROCK1, Ki-67, ICAM-1 and ROCK2,
*Ki-67↓,
*ICAM-1↓,
*cardioP↑, Lycopene is a cardioprotective nutraceutical.
*antiOx↑, Lycopene is a well-known antioxidant.
*NQO1↑, Furthermore, lycopene supplementation improves mRNA expressions of the NQO-1 and HO-1 as antioxidant enzymes.
*HO-1↑,
*TNF-α↓, downregulate inflammatory cytokines (i.e., TNF-α, and IL-1β) in the hippocampus of the mice.
*IL22↓,
*NRF2↑, Lycopene decreased neuronal oxidative damage by activating Nrf2, as well as by inactivating NF-κB translocation in H2O2-related SH-SY5Y cell model
*NF-kB↓,
*MDA↓, significantly reduced the malondialdehyde (MDA)
*Catalase↑, Furthermore, it improved the catalase (CAT), superoxide dismutase (SOD), and GSH levels, and antioxidant capacity [109].
*SOD↑,
*GSH↑,
*cognitive↑, Lycopene administration considerably improved cognitive defects, noticeably reduced MDA levels and elevated GSH-Px activity, and remarkably reduced tau
*tau↓,
*hepatoP↑, Lycopene was also found to be effective against hepatotoxicity by acting as an antioxidant, regulating total glutathione (tGSH) and CAT concentrations
*MMP2↑, It also elevated MMP-2 down-regulation
*AST↓, lowering the liver enzymes levels, like aspartate transaminase (AST), alanine transaminase (ALT), LDL, free fatty acid, and MDA.
*ALAT↓,
*P450↑, Moreover, tomato powder has been shown to have a protective agent against alcohol-induced hepatic injury by inducing cytochrome p450 2E1
*DNAdam↓, lycopene decreased DNA damage
*ROS↓, It has been revealed that they inhibited ROS production, protected antioxidant enzymes, and reversed hepatotoxicity in rats’ liver
*neuroP↑, lycopene consumption relieved cognitive defects, age-related memory loss, neuronal damage, and synaptic dysfunction of the brain.
*memory↑,
*Ca+2↓, Lycopene suppressed the 4-AP-invoked release of glutamate and elevated intra-synaptosomal Ca2+ level.
*Dose↝, an in vivo study revealed that lycopene (6.5 mg/day) was effective against cancer in men [147]. However, lycopene dose should be increased up to 10 mg/day, in the case of advanced PCa.
*Dose↑, lycopene supplementation (15 mg/day, for 12 weeks) in an old aged population improved immune function through increasing natural killer cell activity by 28%
*Dose↝, Finally, according to different epidemiological studies, daily lycopene intake can be suggested to be 2 to 20 mg per day
*toxicity∅, A toxicological study on rats showed the no-observed-adverse-effect level at the highest examined dose (i.e., 1.0% in the diet)
PGE2↓, Lycopene doses of 0, 10, 20, and 30 µM were used to treat human colorectal cancer cell. Prostaglandin E2 (PGE2), and NO levels declined after lycopene administration,
CDK2↓, Treatment with lycopene reduced cell hyperproliferation induced by UVB and ultimately promoted apoptosis and reduced CDK2 and CDK4 complex in SKH-1 hairless mice
CDK4↓,
STAT3↓, lycopene reduced the STAT3 expression in ovarian tissues
NOX↓, (SK-Hep-1) cells and indicated a substantial reduction in NOX activity. Moreover, it inhibits the protein expression of NOX4, NOX4 mRNA and ROS intracellular amounts
NOX4↓,
ROS↓,
*SREBP1↓, Lycopene decreases the fatty acid synthase (FAS), sterol regulatory element-binding protein 1c (SREBP-1c), and Acetyl-CoA carboxylase (ACC1) expression in HFD mice.
*FASN↓,
*ACC↓,


Showing Research Papers: 1 to 50 of 86
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 86

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

CXCR3↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   Bil↝, 1,   Catalase↓, 1,   GPx↓, 1,   GSH↓, 3,   GSH↑, 1,   HO-1↓, 1,   lipid-P↑, 2,   MDA↓, 3,   MDA↑, 1,   NOX4↓, 1,   NRF2↓, 1,   ROS↓, 1,   ROS↑, 12,   SOD↓, 1,   uricA↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

CDC25↓, 1,   FGFR1↓, 2,   MMP↓, 2,   MMP↑, 1,   mtDam↑, 1,   XIAP↓, 2,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 11,   cMyc↓, 3,   Glycolysis↓, 2,   HK2↓, 1,   LDH↓, 1,   LDL↓, 1,   PDK1↓, 1,   PKM2↓, 1,   PPARα↓, 1,   Warburg↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 5,   p‑Akt↓, 2,   Apoptosis↓, 1,   Apoptosis↑, 7,   BAX↓, 1,   BAX↑, 6,   Bcl-2↓, 8,   Bcl-2↑, 1,   Bcl-xL↓, 1,   Casp↑, 2,   Casp1↑, 1,   Casp12↑, 1,   Casp3↑, 7,   Casp7↑, 1,   Casp8↑, 4,   Casp9↑, 3,   cl‑Casp9↑, 1,   cFLIP↓, 1,   CK2↓, 1,   Cyt‑c↑, 7,   DR4↑, 1,   DR5↑, 1,   FADD↑, 2,   Fas↑, 4,   hTERT/TERT↓, 1,   iNOS↓, 1,   JNK↑, 1,   p‑JNK↑, 1,   MAPK↓, 2,   Mcl-1↓, 1,   NOXA↑, 1,   p38↑, 2,   PUMA↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

tumCV↓, 3,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP↑, 1,   eIF2α↑, 1,   p‑eIF2α↑, 1,   ER Stress↑, 4,   GRP78/BiP↑, 2,   p‑PERK↑, 1,   UPR↑, 1,   XBP-1↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1↓, 1,   Beclin-1↑, 2,   BNIP3↑, 1,   LC3‑Ⅱ/LC3‑Ⅰ↓, 1,   LC3II↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

CHK1↓, 1,   DNAdam↑, 3,   P53↑, 5,   PARP↑, 2,   cl‑PARP↑, 3,   PCNA↓, 3,   γH2AX↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK2↓, 2,   CDK4↓, 5,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 4,   cycE/CCNE↑, 1,   P21↑, 6,   TumCCA↑, 8,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

CD133↓, 1,   CDK8↓, 1,   p‑cMET↑, 1,   CSCs↓, 2,   EMT↓, 4,   ERK↓, 6,   FGF↓, 1,   FGFR2↓, 1,   Gli↓, 1,   GSK‐3β↓, 2,   HDAC↓, 2,   HH↓, 1,   HRAS↓, 1,   miR-34a↓, 1,   mTOR↓, 4,   Nestin↓, 1,   NOTCH↓, 2,   NOTCH1↓, 1,   NOTCH1↑, 1,   P90RSK↓, 1,   PI3K↓, 6,   PTEN↑, 1,   RAS↑, 1,   Shh↓, 2,   STAT3↓, 6,   p‑STAT3↓, 2,   TOP1↓, 1,   TRPM7↓, 1,   TumCG↓, 3,   tyrosinase↓, 1,   Wnt↓, 1,  

Migration(tgid=13) ⓘ

AXL↓, 1,   Ca+2↑, 1,   CLDN1↓, 1,   E-cadherin↓, 2,   E-cadherin↑, 2,   F-actin↓, 1,   p‑FAK↓, 1,   Fibronectin↓, 1,   Ki-67↓, 3,   KRAS↓, 1,   MMP-10↓, 1,   MMP1↓, 1,   MMP2↓, 7,   MMP2↑, 1,   MMP9↓, 8,   MMPs↓, 2,   N-cadherin↓, 1,   PDGF↓, 1,   Slug↓, 2,   Smad1↑, 1,   Snail↓, 2,   TET1↑, 1,   TGF-β↓, 1,   TIMP1↑, 1,   TIMP2↑, 1,   TIMP3↑, 1,   TRIB3↑, 1,   TumCI↓, 3,   TumCMig↓, 5,   TumCP↓, 4,   TumMeta↓, 5,   TumMeta↑, 1,   Twist↓, 3,   Vim↓, 2,   ZEB2↓, 1,   β-catenin/ZEB1↓, 3,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 2,   EGFR↓, 3,   Hif1a↓, 4,   VEGF↓, 10,   VEGFR2↓, 2,  

Barriers & Transport(tgid=15) ⓘ

P-gp↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX1↓, 1,   COX2↓, 5,   COX2↑, 1,   CXCc↓, 1,   CXCR4↓, 2,   HMGB1↓, 1,   ICAM-1↓, 1,   IL10↓, 1,   IL1β↓, 2,   IL6↓, 4,   IL8↓, 1,   Inflam↓, 3,   MCP1↓, 1,   NF-kB?, 1,   NF-kB↓, 7,   NF-kB↑, 1,   PGE2↓, 3,   TLR4↓, 1,   TNF-α↓, 4,  

Cellular Microenvironment(tgid=17) ⓘ

NOX↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

AR↓, 1,   CDK6↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 4,   ChemoSen↑, 5,   Dose↝, 3,   eff↑, 7,   RadioS↑, 3,   selectivity↑, 2,  

Clinical Biomarkers(tgid=22) ⓘ

AFP↓, 2,   ALAT↓, 11,   ALP↓, 4,   AR↓, 1,   AST↓, 9,   Bil↝, 1,   BMPs↑, 1,   creat↓, 2,   EGFR↓, 3,   hTERT/TERT↓, 1,   IL6↓, 4,   Ki-67↓, 3,   KRAS↓, 1,   LDH↓, 1,   TG/TAG↓, 1,   TRIB3↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↓, 1,   AntiCan↑, 5,   AntiTum↑, 1,   cardioP↑, 2,   chemoP↑, 5,   chemoPv↑, 1,   hepatoP↑, 6,   neuroP↑, 1,   OS↓, 1,   OS↑, 2,   radioP↑, 1,   RenoP↑, 2,   Weight↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

Sepsis↓, 1,  
Total Targets: 226

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

AntiArt↑, 1,   AntiBio↑, 2,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 18,   Bil↓, 2,   Catalase↑, 17,   Ferroptosis↓, 1,   GPx↓, 1,   GPx↑, 13,   GSH↓, 1,   GSH↑, 21,   GSR↑, 3,   GSTA1↑, 2,   GSTs↑, 2,   HDL↑, 1,   HO-1↑, 9,   Keap1↓, 2,   lipid-P↓, 15,   MDA↓, 20,   MPO↓, 2,   NQO1↑, 4,   NRF2↓, 1,   NRF2↑, 17,   ROS↓, 31,   SIRT3↑, 1,   SOD↓, 1,   SOD↑, 22,   TAC↑, 2,   TBARS↓, 1,   TOS↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↓, 1,   ATP↑, 1,   MMP↑, 1,   OCR↑, 1,   PGC-1α↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ACC↓, 1,   ALAT↓, 38,   AMPK↓, 1,   AMPK↑, 4,   p‑AMPK↑, 1,   cAMP↑, 1,   FASN↓, 1,   glucose↓, 2,   H2S↑, 1,   LDH↓, 9,   LDH↑, 1,   LDL↓, 1,   NAD↓, 1,   NADPH↓, 1,   NADPH↑, 1,   PFK↓, 1,   PPARα↑, 1,   PPARγ↓, 1,   PPARγ↑, 2,   SIRT1↑, 2,   SREBP1↓, 2,  

Cell Death(tgid=5) ⓘ

Akt↓, 2,   Apoptosis↓, 5,   BAX↓, 2,   Bcl-2↓, 1,   Bcl-2↑, 1,   Casp1↓, 1,   Casp3↓, 3,   cl‑Casp3↓, 1,   Casp9↓, 1,   Cyt‑c↓, 1,   Fas↓, 1,   Ferroptosis↓, 1,   GADD34↓, 1,   iNOS↓, 5,   JNK↓, 1,   MAPK↓, 1,   necrosis↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

Ach↑, 1,   AntiThr↑, 1,   other↑, 1,   other↝, 2,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP↓, 3,   ER Stress↓, 2,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1↓, 1,   Beclin-1↑, 1,   LC3II↓, 1,   LC3II↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 1,   P53↓, 1,   cl‑PARP1↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

P21↓, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

GSK‐3β↓, 2,   mTOR↓, 1,   mTOR↑, 1,   Nestin↑, 1,   NOTCH1↑, 1,   PI3K↓, 2,   PI3K↑, 1,   SOX2↑, 1,   p‑STAT3↓, 1,   TRPM7↓, 1,  

Migration(tgid=13) ⓘ

5LO↓, 1,   AntiAg↑, 2,   Ca+2↓, 2,   CEA↓, 1,   COL3A1↓, 1,   Ki-67↓, 1,   Ki-67↑, 1,   MMP13↓, 1,   MMP2↑, 1,   MMP3↓, 1,   MMP9↑, 1,   p‑Rac1↓, 1,   ROCK1↓, 1,   SMAD3↓, 1,   TGF-β1↓, 1,   TXNIP↓, 1,   ZO-1↑, 1,   α-SMA↓, 2,  

Angiogenesis & Vasculature(tgid=14) ⓘ

ATF4↓, 2,   Hif1a↓, 1,   NO↓, 6,   VEGF↓, 2,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,   GastroP↑, 1,   P-gp↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD4+↑, 1,   COX2↓, 7,   COX2↑, 1,   CRP↓, 1,   ICAM-1↓, 2,   IFN-γ↓, 3,   IKKα↓, 1,   IKKα↑, 1,   IL10↓, 2,   IL10↑, 2,   IL17↓, 2,   IL18↓, 1,   IL1β↓, 6,   IL2↓, 1,   IL22↓, 1,   IL6↓, 9,   Imm↓, 1,   Imm↑, 7,   Inflam↓, 25,   Inflam↑, 1,   p‑JAK2↓, 1,   MCP1↓, 1,   MyD88↓, 2,   NF-kB↓, 15,   PGE2↓, 5,   TLR4↓, 3,   TNF-α↓, 14,  

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 2,   BDNF↓, 1,   BDNF↑, 2,   MAOA↓, 1,   NGF↑, 1,   tau↓, 1,   TrkB↑, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 3,   BACE↓, 1,   MAOB↓, 1,   NLRP3↓, 5,   PP2A↑, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

CYP19↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 4,   BioAv↑, 2,   BioAv↝, 2,   Dose↑, 1,   Dose↝, 8,   eff↑, 5,   eff↝, 1,   Half-Life↝, 1,   P450↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 38,   ALP↓, 12,   AST↓, 41,   BG↓, 1,   Bil↓, 2,   BP↓, 2,   CEA↓, 1,   creat↓, 2,   CRP↓, 1,   GutMicro↑, 5,   IL6↓, 9,   Ki-67↓, 1,   Ki-67↑, 1,   LDH↓, 9,   LDH↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiAge↑, 1,   AntiCan↑, 4,   AntiDiabetic↑, 6,   AntiTum↑, 1,   cardioP↑, 11,   chemoP↑, 1,   cognitive↑, 5,   hepatoP↑, 32,   memory↑, 6,   motorD↑, 2,   neuroP↑, 17,   Obesity↓, 4,   Pain↓, 1,   RenoP↑, 5,   toxicity↓, 3,   toxicity↝, 2,   toxicity∅, 3,   Weight↓, 1,   Wound Healing↓, 1,   Wound Healing↑, 2,  

Infection & Microbiome(tgid=24) ⓘ

Bacteria↓, 5,   Sepsis↓, 1,  
Total Targets: 207

Scientific Paper Hit Count for: AST, Aspartate Aminotransferase
5 Carvacrol
5 Selenium NanoParticles
5 Silymarin (Milk Thistle) silibinin
5 Thymoquinone
4 Silver-NanoParticles
3 Baicalein
3 Centella asiatica / Gotu kola → asiaticoside
3 Emodin
3 Shikonin
2 Curcumin
2 Boron
2 Selenium
2 Chemotherapy
2 Dandelion Root
2 Hydrogen Gas
2 Honokiol
2 Moringa oleifera
2 Propolis -bee glue
2 Rosmarinic acid
2 Sulforaphane (mainly Broccoli)
1 1,8-Cineole
1 Resveratrol
1 Allicin (mainly Garlic)
1 Alpha-Lipoic-Acid
1 Ashwagandha(Withaferin A)
1 Berberine
1 Biochanin A
1 Betulinic acid
1 Boswellia (frankincense)
1 α-Bisabolol / Chamomile oil
1 Caffeic acid
1 Carnosic acid
1 Thymol-Thymus vulgaris
1 Cynanbungeigenin C (CBC) and D (CBD)
1 Celastrol
1 Chrysin
1 Crocetin
1 Carvone
1 diet Fermented Foods
1 diet Short Term Fasting
1 Ellagic acid
1 Eugenol
1 Ferulic acid
1 Shilajit/Fulvic Acid
1 Luteolin
1 Lycopene
1 Magnetic Field Rotating
1 Magnetic Fields
1 Piperine
1 Quercetin
1 Rutin
1 Salvia officinalis
1 chitosan
1 polyethylene glycol
1 Cisplatin
1 Ursolic acid
1 Vitamin B5,Pantothenic Acid
1 Vitamin C (Ascorbic Acid)
1 Vitamin K2
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#:691  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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