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Updated: Feb 4, 2026

Systematic Scoring Analysis for Intestinal Inflammation in a Murine Dextran Sodium Sulfate-Induced Colitis Model
Published on: February 14, 2021
Ginsenoside Rb3 Mitigates Murine Ulcerative Colitis by Modulating Intestinal Microflora and Short-Chain Fatty Acids
Wei Zhang1, Qiben Wang2, Tianjie Zhang1
1Department of Physiology, School of Basic Medicine, Xiangnan University, Chenzhou, Hunan 423000, P.R. China.
Ginsenoside Rb3 (GR3) effectively treats colitis in mice by restoring gut microbiota balance, strengthening the intestinal barrier, and reducing inflammation. This natural compound offers a promising therapeutic approach for inflammatory bowel disease (IBD).
Area of Science:
- Gastroenterology
- Microbiology
- Pharmacology
Background:
- Inflammatory bowel disease (IBD) progression is linked to ecological dysregulation in the gut.
- Dextran sulfate sodium (DSS)-induced colitis is a common model for studying IBD.
Purpose of the Study:
- To investigate the therapeutic potential of ginsenoside Rb3 (GR3) in ameliorating DSS-induced colitis.
- To determine if GR3 exerts its effects by modulating the gut microbiota.
Main Methods:
- Oral administration of GR3 (5 mg/kg) to mice with DSS-induced colitis.
- Evaluation of therapeutic effects using histological analysis, ELISA, and Western blotting.
- Assessment of gut microbiota composition and short-chain fatty acid (SCFA) metabolism.
Main Results:
- GR3 treatment significantly alleviated colitis symptoms, including weight loss, diarrhea, and colonic shortening.
- GR3 elevated tight junction protein expression (occludin, zonula occludens-1), reducing inflammatory cell infiltration and cytokine levels (TNF-α, IL-1β, IL-15, IL-17A, IL-6).
- GR3 modulated gut microbiota, increasing *Lactobacillus* and decreasing *Bacillus*, and elevated acetic and butyric acid levels.
Conclusions:
- Ginsenoside Rb3 ameliorates DSS-induced colitis by improving the intestinal barrier function and reducing inflammation.
- GR3's therapeutic effects are associated with reshaping the gut microbiota and restoring SCFA metabolism.
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