ArticleDigestive diseases and sciences2008
Green-tea polyphenols downregulate cyclooxygenase and Bcl-2 activity in acetaminophen-induced hepatotoxicity.
Article in Digestive diseases and sciences, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 56 citations in OpenAlex.
- Cardioprotective and Hepatoprotective Potential of Silymarin in Paracetamol-Induced Oxidative Stress.Pharmaceutics · 2024Article
- Hepatoprotective Effects of Radish (Nutrients · 2022Article
- Article
- Diacerein counteracts acetaminophen-induced hepatotoxicity in mice via targeting NLRP3/caspase-1/IL-1β and IL-4/MCP-1 signaling pathways.Archives of pharmacal research · 2022Article
- Creatinine accelerates APAP-induced liver damage by increasing oxidative stress through ROS/JNK signaling pathway.Frontiers in pharmacology · 2022Article
- Extract ofMolecules (Basel, Switzerland) · 2021Article
- Cellular Defensive Mechanisms of Tea Polyphenols: Structure-Activity Relationship.International journal of molecular sciences · 2021Review
- Epigallocatechin-3-Gallate Reduces Hepatic Oxidative Stress and Lowers CYP-Mediated Bioactivation and Toxicity of Acetaminophen in Rats.Nutrients · 2019Article
- Epigallocatechin-3-Gallate Toxicity in Children: A Potential and Current Toxicological Event in the Differential Diagnosis With Virus-Triggered Fulminant Hepatic Failure.Frontiers in pharmacology · 2019Review
- Ginsenoside Rk1 ameliorates paracetamol-induced hepatotoxicity in mice through inhibition of inflammation, oxidative stress, nitrative stress and apoptosis.Journal of ginseng research · 2019Article
- Bioavailability of Tea Catechins and Its Improvement.Molecules (Basel, Switzerland) · 2018Review
- Association of antioxidant nutraceuticals and acetaminophen (paracetamol): Friend or foe?Journal of food and drug analysis · 2018Review
- Treatment of inflammatory bowel disease via green tea polyphenols: possible application and protective approaches.Inflammopharmacology · 2018Review
- Chronic Inflammatory Diseases and Green Tea Polyphenols.Nutrients · 2017Review
- Ameliorative Effects and Possible Molecular Mechanism of Action of Black Ginseng (Panax ginseng) on Acetaminophen-Mediated Liver Injury.Molecules (Basel, Switzerland) · 2017Article
- Overexpression of Aldose Reductase Render Mouse Hepatocytes More Sensitive to Acetaminophen Induced Oxidative Stress and Cell Death.Indian journal of clinical biochemistry : IJCB · 2016Article
- In vitro toxicity of epigallocatechin gallate in rat liver mitochondria and hepatocytes.Oxidative medicine and cellular longevity · 2015Article
- Protective effect of pioglitazone, a PPARγ agonist against acetaminophen-induced hepatotoxicity in rats.Molecular and cellular biochemistry · 2014Article
- Protective effect of Baccharis trimera extract on acute hepatic injury in a model of inflammation induced by acetaminophen.Mediators of inflammation · 2014Article
- Green Tea Polyphenols and Sulfasalazine have Parallel Anti-Inflammatory Properties in Colitis Models.Frontiers in immunology · 2013Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Acetaminophen (APAP) elicits hepatotoxicity via multifactorial pathways, including increased apoptosis, cyclooxygenase (Cox-2) generation, reactive metabolite release, and glutathione (GSH) depletion. We previously showed that mice that consumed different antioxidants in their diets were protected against APAP-induced hepatotoxicity. We therefore further investigated the mechanisms by which green-tea polyphenols (GrTP) protect against APAP-induced hepatic damage. Mice were administered a diet supplemented with GrTP or vehicle for 5 consecutive days followed by intraperitoneal (IP) injection of a toxic dose of APAP or sham. APAP administration upregulated Cox-2 and B-cell lymphoma-2 (Bcl-2) production and had an effect, albeit minor, on Cox-1 and Fas expression in hepatic tissue. GrTP supplementation normalized APAP induced Cox-2 expression and Bcl-2 activation (P < 0.01), as evidenced by immunohistochemistry and Western blot analyses. Similarly, APAP administration elicited marked depletion (99%) in hepatic reduced GSH (rGSH) and endogenous S-adenosylmethionine (SAMe) concentrations (twofold) when compared with sham. APAP also caused severe centrilobular apoptosis and necrosis accompanied by leukocyte infiltration and marked elevations in the hepatic enzyme, alanine aminotransferase (ALT) released from damaged hepatocytes, and cytokine tumor necrosis factor alpha (TNF-alpha). GrTP improved hepatic histopathology (P < 0.01) and attenuated ALT activity (P < 0.05) and the depletion of rGSH (P < 0.05). In conclusion, GrTP supplementation attenuated hepatotoxicity by normalizing Cox-2 and Bcl-2 activation, suggesting a potential use for GrTP in treatng APAP toxicity.
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