ArticleAmerican journal of translational research2026
Polydatin ameliorates alcohol-induced gastric ulcer by inhibiting CASP3-mediated apoptosis.
Article in American journal of translational research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveTo explore the protection of polydatin (PD) against alcoholic gastric ulcer (AIGU) in mice and the related molecular pathways.
methodsPD targets related to AIGU were predicted using network pharmacology, and Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed. A mouse gastric ulcer model was established via intragastric administration of ethanol, and the effects of PD on gastric mucosal morphology, oxidative damage, inflammation, and apoptosis-related proteins were evaluated; In vitro, the effects of PD on ethanol-injured GES-1 cells were further assessed in the presence or absence of the caspase-3 inhibitor Z-DEVD-FMK.
resultsNetwork pharmacology showed that PD exerts its effects through apoptosis-related pathways. In vivo, PD significantly alleviated gastric mucosal injury, reduced the levels of malondialdehyde and pro-inflammatory cytokines, and increased the activities of antioxidant enzymes. It up-regulated mucosal protection factors (epidermal growth factor, prostaglandin E
conclusionPD exerts antioxidant, anti-inflammatory, and anti-apoptotic effects against AIGU, especially inhibiting CASP3-mediated apoptosis, which shows its potential as a natural gastric protection therapy.
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