# Ginsenoside Rb3 Mitigates Murine Ulcerative Colitis by Modulating Intestinal Microflora and Short-Chain Fatty Acids

## TL;DR

Ginsenoside Rb3 reduces colitis in mice by improving gut bacteria and reducing inflammation.

## Contribution

GR3 is shown to reshape gut microbiota and alleviate colitis through specific microbial and metabolic changes.

## Key findings

- GR3 treatment reduced colitis symptoms like weight loss and colonic shortening in mice.
- GR3 increased tight junction proteins and decreased inflammatory cytokines in colitis mice.
- GR3 boosted Lactobacillus and short-chain fatty acids like butyric acid, improving gut health.

## Abstract

Ecological dysregulation leads to the progression of inflammatory bowel disease (IBD). The present study was designed to evaluate whether ginsenoside Rb3 (GR3) ameliorates dextran sulfate sodium (DSS)-induced colitis by modifying the microbiota. The results revealed that GR3 treatment with oral doses of 5 mg/kg suppressed DSS-induced colitis in mice, and its effects were evaluated using a combination of histological analysis, enzyme-linked immunosorbent assays (ELISA), and Western blotting. This was evidenced by a significant attenuation of symptoms such as weight loss, diarrhea, hematochezia, and colonic shortening in the DSS-induced colitis mice. Furthermore, GR3 treatment remarkably elevated the expression of tight junction proteins (occludin and zonula occludens-1) while reducing both inflammatory cell infiltration and inflammatory cytokine concentrations (TNF-α, IL-1β, IL-15, IL-17A, and IL-6). Intriguingly, GR3 treatment also mitigated DSS-induced intestinal dysbiosis by prominently increasing the proliferation of Lactobacillus and decreasing the relative abundance of Bacillus. Additionally, GR3 treatment significantly modified the metabolism of short-chain fatty acids in colitis mice, especially elevating the levels of acetic acid and butyric acid. These findings suggest that GR3 ameliorates colitis by reshaping the gut microbiota and improving the intestinal barrier and inflammation.