Myricitrin enhances allocholic acid metabolism to restore gut barrier and alleviate ulcerative colitis in mice via the microbiota-metabolite-host axis

Inflammatory bowel disease (IBD) is closely associated with gut microbiota imbalance and intestinal barrier dysfunction. Bayberries improve intestinal health, with myricitrin (MYRR) as their main active component. However, the mechanism by which MYRR modulates the “microbiota–metabolite–host” axis to alleviate ulcerative colitis remains unclear. This study employs a dextran sodium sulfate (DSS)-induced colitis mouse model, integrating metagenomics, metabolomics, and colonic organoid cultures to explore MYRR's effects. The results demonstrate that MYRR alleviates colitis symptoms and restores the expression of key intestinal barrier proteins, MUC2 and occludin. Multi-omics analysis reveals that MYRR reshapes the gut microbiota by enriching beneficial bacteria and modulating bile acid metabolism, particularly allocholic acid (ACA), in both serum and feces. In vitro intestinal organoid experiments further confirm that ACA enhances MUC2 expression. In conclusion, MYRR protects against colitis by regulating the “microbiota–metabolite–intestinal barrier” axis, offering a theoretical foundation for microbiota-based therapeutic strategies for IBD.