Rosmarinic acid prevents dextran sulfate sodium-induced ulcerative colitis in mice by enhancing the function of the intestinal barrier and preserving intestinal homeostasis

Rosmarinic acid (RA) is a natural phenolic acid with multiple biological and pharmacological properties. However, its protective effect on ulcerative colitis (UC) remains uncertain. This study aims to explore the protective ability and potential mechanism of RA on UC, focusing on the intestinal barrier and homeostasis. UC mice model was established through the induction by dextran sulfate sodium (DSS) of 2.5%, and the progression of the UC after RA treatment was monitored using clinical manifestations, histopathological examination, and biochemical analysis. The mice’s composition of intestinal flora was assessed through 16S rRNA sequencing methods, while the concentrations of short-chain fatty acids (SCFAs) and bile acids (BAs) were analyzed using targeted metabolomics. The findings demonstrated that RA could prevent a decrease in body weight, reduce the scores of disease activity index (DAI), shorten colon length, and restore the claudin-1, zonula occludens-1 (ZO-1), and occludin levels in UC mice. Furthermore, RA effectively suppressed intestinal inflammation, modulated the compositin of gut microbiota, and influenced the levels of SCFAs and BAs. Hence, RA could offer therapeutic benefits for UC mice by enhancing intestinal barrier function and preserving intestinal homeostasis. Given the availability of scientific evidence, it may serve as a preventive agent or remedy for UC.