Amentoflavone ameliorates DSS-induced ulcerative colitis via gut microbiota-bile acid metabolism axis modulation

Amentoflavone (AMF) has anti-inflammatory, antibacterial, and antioxidant properties. However, the effect and underlying mechanisms of AMF on ulcerative colitis (UC) are unclear. This study aimed to examine the protective effects and regulatory mechanisms of AMF in UC in rats. AMF alleviates UC by inhibiting the spleen index, relieving colon shortening, reducing the disease activity index and reversing pathological injury of the colon tissue. Through 16 s high-throughput sequencing technology and targeted metabolomics methods, AMF was found to reconstruct intestinal microorganisms and regulate the homeostasis of bile acid metabolites. Additionally, AMF protects intestinal barrier function by activating bile acid receptors (TGR5 and FXR), and regulating tight junction proteins (ZO-1 and occludin). In conclusion, the therapeutic mechanism of AMF is mainly attributed to the activation of the gut microbiota-bile acid axis. These findings contribute to mechanistic research and drug development for AMF intervention in patients with UC. • Amentoflavone can prevent ulcerative colitis by modulating gut microbiota and its bile acid metabolites. • Amentoflavone protectes intestinal barrier function by activating bile acid receptors and regulating tight junction proteins.