Bergenin suppresses the changes of gut microbiota and colitis induced by dextran sulfate sodium in KM mice

To investigate bergenin's (BE) modulatory effects on gut microbiota dysbiosis and its therapeutic mechanisms in dextran sulfate sodium (DSS)-induced colitis. Kunming mice ( n = 18) were randomized into Control, DSS (2.5 % DSS, 7 days), and DSS + BE (50 mg/kg/day) groups. Disease activity index (DAI), histopathology, and 16S rRNA sequencing of cecal microbiota were analyzed. Inflammatory markers (TLR4, α-SMA, iNOS) and epithelial proliferation (BrdU) were assessed. BE significantly attenuated colitis severity versus DSS group: reduced weight loss (23.1 % vs. 41.5 %, P < 0.05), lowered DAI scores (8.2 vs. 14.7, P < 0.01), and improved histopathology (2.1 vs. 4.8, P < 0.01). BE restored microbial α-diversity (Shannon index: 3.2 ± 0.4 vs. 2.1 ± 0.6, P < 0.01) and specifically increased anti-inflammatory Barnesiella abundance (4.2 % → 11.7 %, P < 0.01). Beta-diversity analysis revealed BE maintained microbiota structural stability (DSS + BE vs. Control dissimilarity <16 % vs. DSS >88 % at genus level). BE suppressed DSS-induced TLR4 overexpression and restored colonic epithelial proliferation (BrdU). Bergenin ameliorates DSS-colitis by restoring gut microbiota homeostasis (notably enriching Barnesiella ), suppressing TLR4-mediated inflammation, and promoting epithelial repair, highlighting its potential as an IBD therapeutic. • First study on bergenin's anti-diarrheal mechanism in colonitis via NF-κB inhibition. • Bergenin regulates gut microbiota composition, linking dysbiosis to diarrhea treatment. • Validation of Bergenia purpurascens as functional food/herb with anti-inflammatory potential. • Elucidates natural product chemistry: bergenin's dual role in microbial modulation and cellular signaling.