β-ionone prevents dextran sulfate sodium-induced ulcerative colitis and modulates gut microbiota in mice

β-ionone has various biological activities, such as anti-inflammatory, antimicrobial, and anticancer effects. The pathogenesis of ulcerative colitis is correlated with immune dysfunction, intestinal barrier damage, and gut microbiota imbalance. However, whether β-ionone has preventive efficacy against ulcerative colitis is unknown. This study investigated the effect of β-ionone on dextran sulfate sodium-induced ulcerative colitis and the underlying molecular mechanisms involved. The ulcerative colitis mouse model was induced by 1.5% dextran sulfate sodium for 10 d. Meanwhile, 200 mg/kg β-ionone was administrated to the mice. Body weight, colon length, colon tissue pathology, colon tissue inflammatory cytokines, colonic oxidative stress, and barrier function were assessed. The composition and structure of gut microbiota were profiled using 16S rRNA sequencing. The results showed that β-ionone supplementation effectively prevented ulcerative colitis by ameliorating colonic tissue damage, reducing inflammatory phenomena, and protecting the colonic epithelial mucosal barrier. β-ionone also protected mice from dextran sulfate sodium-induced gut microbiota disturbance by modifying the overall structure and function of the gut microbiota community and increasing the relative abundance of beneficial gut microbiota. The Spearman correlation analysis revealed that the changes in abundance of the gut microbiota were correlated with ulcerative colitis-related indicators. Overall, this study demonstrated that β-ionone has a preventive effect on ulcerative colitis in mice, and the underlying mechanism may be associated with the protection of the gut barrier and regulation of the gut microbiota. These results are conducive to promoting clinical trials and product development of β-ionone for the prevention and treatment of ulcerative colitis.