Abstract

Ulcerative colitis (UC) is one of the most prevalent inflammatory bowel diseases (IBD) worldwide, while oat β-glucan has been shown to suppress the progress of colitis in UC mice. However, the underlying mechanism of oat β-glucan in ameliorating colitis is unclear and the role of gut microbiota in the protective effect of oat β-glucan against colitis remains unknown. In the present study, we aim to investigate the effect of oat β-glucan on gut microbiota in colitis mice and explore the health effect related mechanism. Dextran sulfate sodium (DSS) was used to induce the colitis model in mice. The results showed that β-glucan treatment attenuated hematochezia, splenomegaly and colon shortening in colitis mice. Histological evaluation of H&E and TUNEL staining showed that β-glucan treatment suppressed DSS-induced colonic inflammatory infiltration and reduced cell apoptosis levels of colon tissues. mRNA expression levels of the pro-inflammatory factors were also significantly reduced in the β-glucan group. Moreover, β-glucan treatment increased the protein and mRNA expression levels of tight junction proteins. Analysis of gut microbiota community showed that β-glucan treatment modulated gut microbial composition and structure at the OTU level in colitis mice. Further analysis of gut microbial metabolism revealed that β-glucan treatment significantly increased acetate, propionate and butyrate concentrations, and affected microbial metabolome in colitis mice. Notably, the increased acetate and propionate concentrations could directly affect pro-inflammatory factor expression levels and tight junction protein levels. In contrast, the changes in metabolic profiles affected pro-inflammatory factor levels and thus affected tight junction protein levels. Overall, our study revealed that oat β-glucan ameliorated DSS-induced colitis in mice simultaneously through regulating gut-derived short-chain fatty acids (SCFAs) and microbial metabolic biomarkers. Our study demonstrated that oat β-glucan could be an effective nutritional intervention strategy towards targeting gut microbiota metabolism for ameliorating colitis.

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