ArticleFrontiers in pharmacology2025
Resveratrol targeting MDM2/P53/PUMA axis to inhibit colonocyte apoptosis in DSS-induced ulcerative colitis mice.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed.
- Multi-Dimensional Mechanisms and Druggability Optimization Strategies of Active Ingredients from Traditional Chinese Medicine in the Treatment of Ulcerative Colitis.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Dysregulated programmed cell death of intestinal epithelial cells in ulcerative colitis: Molecular mechanisms and novel therapeutic interventions (Review).International journal of molecular medicine · 2025Review
Corrections and comments
- Erratum issued
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Resveratrol, a naturally occurring polyphenolic compound found in grapes, berries, and traditional medicinal plants like Polygonum cuspidatum, has been used for centuries in traditional medicine systems for its anti-inflammatory, antioxidant, and cardioprotective properties. Ulcerative colitis (UC), a chronic inflammatory bowel disease, is characterized by intestinal barrier disruption due to excessive colonocyte apoptosis, leading to increased permeability and inflammation. Targeting apoptosis is a critical therapeutic strategy for UC. Aim of the study: This study aims to investigate the therapeutic potential of Resveratrol in ulcerative colitis (UC) by targeting excessive colonocyte apoptosis and intestinal barrier dysfunction. Specifically, we seek to elucidate the mechanisms through which Resveratrol modulates apoptosis-related pathways and evaluate its efficacy in restoring intestinal homeostasis and mitigating UC progression in both Materials and Methods: We used dextran sulfate sodium (DSS) to induce UC in a mouse model. Colonic damage was assessed through colonic length measurement, histological examination, and immunofluorescence staining. Single-cell sequencing was employed to explore changes in the colonic immune microenvironment and cellular signaling pathways after Resveratrol treatment. Results: Resveratrol treatment effectively repaired colonic damage in the UC mouse model by significantly increasing colon length, reducing inflammatory cell infiltration, and mitigating mucosal injury. Single-cell sequencing revealed that Resveratrol primarily targeted colonocytes, decreasing genes related to apoptosis and the P53 pathway. Conclusion: Resveratrol is an effective treatment for DSS-induced UC, primarily by inhibiting excessive apoptosis in colonocytes through the MDM2/P53/PUMA axis. MDM2 presents a promising therapeutic target for UC treatment.
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