Sodium Butyrate Alleviates Mouse Colitis by Regulating Gut Microbiota Dysbiosis

Simple Summary Inflammatory bowel disease (IBD) is extremely harmful to animal health and can affect animal growth and production. Dextran sulfate sodium (DSS) can cause IBD in animals, resulting in diarrhea and bloody stools. The present study aimed to determine whether oral sodium butyrate can relieve DSS-induced colitis in mice. By using histological evaluation (H&E) staining technology and 16S rRNA sequence analysis, we found that the severity of colitis in mice receiving oral sodium butyrate was reduced, and the composition of gut microbiota was changed. These results indicate that sodium butyrate can relieve DSS-induced colitis in mice by restoring the balance of gut microbiota dysbiosis. Inflammatory bowel disease (IBD) develops as a result of complicated interactions between genetic susceptibility, excessive innate immunity, and environmental factors, which are mainly related to the gut microbiota. The present study aimed to elucidate the protective effects and underlying mechanisms of a short-chain fatty acid salt, sodium butyrate, on colonic inflammation induced by dextran sulfate sodium (DSS) in mice. Pretreatment with sodium butyrate attenuated colitis, as demonstrated by the decreased disease activity index (DAI), colon length shortening, spleen tumidness, and histopathology scores, while maintaining intestinal barrier integrity, as observed by H&E staining and electron microscopy. 16S rRNA sequence analysis revealed that sodium butyrate caused a remarkable alteration of the gut microbiota.Bacteroides,Lachnospiraceae, theLachnospiraceae NK4A136group, andRuminiclostridium 6presented dramatic differences after sodium butyrate supplementation. This work verifies that sodium butyrate can improve mouse colitis via microbe-host interactions by regulating the microbial community. Taken together, the findings demonstrate that sodium butyrate shows great potential as a probiotic agent for ameliorating colitis.