Polydatin ameliorates alcohol-induced gastric ulcer by inhibiting CASP3-mediated apoptosis

23/09/2026

AI Summary

Polydatin significantly alleviates ethanol-induced gastric mucosal injury in mice by reducing oxidative stress and inflammation, and increasing antioxidant enzymes and protective factors.
Polydatin modulates apoptosis proteins, increasing BCL-2 and decreasing BAX and CASP3, indicating anti-apoptotic action.
In vitro, Z-DEVD-FMK mimicked PD's protection; no additive effect with combined treatment, implying PD primarily inhibits CASP3-mediated apoptosis.

TL;DR (AI Generated)

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.

In vitro, PD protects gastric mucosal epithelial cells from apoptosis; the caspase-3 inhibitor Z-DEVD-FMK alone mimicked the protective effects of PD, and combined treatment with PD and Z-DEVD-FMK did not produce a markedly additive effect, suggesting that PD exerts its anti-apoptotic effect primarily through inhibition of caspase-3 (CASP3)-mediated apoptosis.

CONCLUSION: PD 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.

Basic summary

Am J Transl Res. 2026 Aug 15;18(8):6850-6865. doi: 10.62347/ECGE1624. eCollection 2026.

ABSTRACT

OBJECTIVE: To explore the protection of polydatin (PD) against alcoholic gastric ulcer (AIGU) in mice and the related molecular pathways.

METHODS: PD 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.

RESULTS: Network 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 E₂) and regulates apoptosis-related proteins (B-cell lymphoma-2, B-cell lymphoma-2-associated X protein, cysteinyl aspartate-specific proteinase-3). In vitro, PD protects gastric mucosal epithelial cells from apoptosis; the caspase-3 inhibitor Z-DEVD-FMK alone mimicked the protective effects of PD, and combined treatment with PD and Z-DEVD-FMK did not produce a markedly additive effect, suggesting that PD exerts its anti-apoptotic effect primarily through inhibition of caspase-3 (CASP3)-mediated apoptosis.

PMID:42769162 | PMC:PMC13590680 | DOI:10.62347/ECGE1624

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