ArticleFrontiers in pharmacology2025
Gallic acid mitigates high-fat and high-carbohydrate diet-induced steatohepatitis by modulating the IRF6/PPARγ signaling pathway.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed.
- Vegetal choline supplementation modulates hepatic metabolism and immune-related transcriptional responses in broilers.Poultry science · 2026Article
- Sequential Fractionation ofFoods (Basel, Switzerland) · 2026Article
- Article
- Interferon Regulatory Factors in Alcohol-Associated Liver Disease: Cell-Type Programs, Danger Signaling, and Therapeutic Opportunities.Current issues in molecular biology · 2026Review
- D-limonene ameliorates metabolic dysfunction-associated steatotic liver disease by inhibiting the PPARγ/SCD-1 pathway and improving lipid metabolism disorders.Frontiers in pharmacology · 2026Article
- Dynamics of Physicochemical Properties, Flavor, and Bioactive Components inFoods (Basel, Switzerland) · 2025Article
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14 authors.
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Abstract
Gallic acid (GA), a natural organic phenolic compound, is an abundant plant food bioactive substance present in many medicinal herbs. GA has anti-oxidative, anti-inflammatory and anticancer activities on multiple metabolic disorders. The present study was carried out to uncover the alleviating effects of GA on metabolic dysfunction-associated steatohepatitis (MASH) and the underlying mechanisms of its action. In this study, a mouse model of MASH induced by high-fat and high-carbohydrate diet was used to test the impact of GA on metabolic disorders. We found that GA administration attenuated obesity and fatty liver, relieved insulin resistance, and mitigated hepatic steatosis, inflammation and liver injury. Transcriptome sequencing (RNA-seq) of mouse liver tissues identified 154 differentially expressed genes (DEGs) among the NCD, HFHC, and GA groups. Bioinformatic analysis of these DEGs revealed significant enrichment in lipid metabolism function and the PPARγ signaling pathway, which were further validated. Overexpression of PPARγ significantly reduced the therapeutic effect of GA both
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