Abstract：Objective: To investigate the ameliorative effect of ginsenoside Rg1 (RG1)on mice with inflammatory bowel disease and its effect on peroxisome proliferator-activated receptor gamma (PPARγ) signaling pathway. Methods: Ulcerative colitis (UC) mouse model was induced by dextran sulfate sodium (DSS). Mice were randomly divided into control group, model group, Rg1-L group, Rg1-M group, and Rg1-H group, with 12 rats in each group. After 10 days of oral administration of RG1,Histopathological analysis was performed using hematoxylin and eosin (HE) and Alcian Blue-Periodic Acid-Schiff (AB-PAS) staining. Oxidative stress-related markers, intestinal injury markers, and inflammatory cytokines were analyzed using respective kits. Immunohistochemistry was used to assess the expression of tight junction proteins. Western blotting was performed to measure PPARγ expression. Results: Compared to the model group, RG1 treatment did not significantly change body weight but significantly increased colon length (P < 0.05). RG1 significantly improved DSS-induced colon tissue damage and repaired the destruction of goblet cells and the intestinal mucus layer. RG1 treatment significantly reduced the levels of nitric oxide (NO) and malondialdehyde (MDA) in colon tissue (P < 0.05), and significantly increased the activity of antioxidant enzymes (glutathione [GSH], catalase [CAT], superoxide dismutase [SOD]) (P < 0.05). RG1 significantly lowered serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels (P < 0.05). Additionally, RG1 significantly inhibited the levels of interleukin-6 (IL-6), interleukin-1 beta (IL-1β), and tumor necrosis factor alpha (TNF-α) (P < 0.05). RG1 treatment increased the expression of Claudin-1, Occludin, and zonula occludens-1 (ZO-1) in the colon (P < 0.05), thereby improving intestinal barrier integrity. RG1 significantly elevated immunoglobulin A (IgA) and immunoglobulin E (IgE) levels (P < 0.05) and upregulated PPARγ expression (P < 0.05), suggesting a protective effect through immune modulation. Furthermore, RG1 significantly increased the concentrations of short-chain fatty acids (SCFAs) (acetate, propionate, butyrate, etc.) in the cecal contents of mice (P < 0.05). Conclusion: RG1 can decrease DSS-induced intestinal barrier damage via reducing oxidative stress and modulating SCFA, and activating the PPARγsignaling pathway.
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2025, Vol. 31 
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