ArticleMolecular biology reports2025
Resveratrol ameliorates CCl
Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Natural Product Treatment for Metabolic Dysfunction-Associated Steatotic Liver Disease: Targeted Mitochondrial Quality Control.Drug design, development and therapy · 2026Review
- Diet for the prevention and treatment of Parkinson's disease.Frontiers in nutrition · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOverexposure to hepatotoxins is a frequent cause of acute liver injury (ALI). This study aimed to investigate the protective effect of resveratrol (RSV) against carbon tetrachloride (CCl₄)-induced ALI and its underlying mechanisms.
methodsIn vitro, four hepatic cell lines (HepG2, Huh7, Hepa1-6, and AML12) were pretreated with RSV (10, 20, or 40 µg/mL) before CCl₄ exposure. Cell viability, reactive oxygen species (ROS) levels, and mitophagy-related protein expression were assessed. In vivo, mice were orally administered RSV (10-40 mg/kg) for 7 days prior to CCl₄-induced ALI. Liver histopathological, liver function, oxidative stress markers, and apoptosis were measured.
resultsRSV significantly attenuated CCl₄-induced cytotoxicity and ROS overproduction in vitro. It activated the expression of PTEN-induced putative kinase 1 (PINK1)/parkin RBR E3 ubiquitin protein ligase (Parkin)-dependent mitophagy, as indicated by upregulated Parkin, PINK1 and LC3-II (microtubule associated protein 1 light chain 3 beta), and reduced p62 expression. In vivo, RSV ameliorated CCl₄-induced ALI, reducing histopathological damage and serum alanine aminotransferase (ALT) / aspartate aminotransferase (AST) levels. RSV enhanced hepatic antioxidant capacity and decreased lipid peroxidation. Furthermore, RSV reduced hepatocyte apoptosis and consistently activated the PINK1/Parkin mitophagy pathway in liver tissues. Both in vitro and in vivo, RSV with the high dose exhibits the most potent effects.
conclusionsThese findings demonstrate that RSV, particularly at the high dose exerts hepatoprotective effects against CCl₄-induced ALI, partly by activating PINK1/Parkin-dependent mitophagy and alleviating oxidative stress. This highlights mitophagy's critical role in RSV-mediated protection and offers novel insights into its therapeutic mechanisms.
Indexed as
Identifiers
41196396What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.