Ulcerative colitis (UC) is a chronic and recurrent inflammatory bowel disease, and the intestinal barrier is an important line of defense against intestinal disease. Herein, we investigated the effect of JM1 at different doses (1 × 10, 1 × 10, 1 × 10 CFU/day) on colitis mice and explored the possible mechanism. The results showed that JM1 alleviated DSS-induced colitis in mice, with reductions in disease activity index (DAI), histological scores and myeloperoxidase activity as well as alleviation of colonic shortening. Furthermore, JM1 regulated the levels of inflammatory cytokines TNF-α, IL-6, IL-1β, and IL-10; restored the expression of Claudin-3, Occludin, ZO-1, and MUC2; and increased the number of goblet cells and acidic mucin. The 16S rDNA sequencing results indicated that intervention with JM1 balanced the gut microbiota structure by elevating the abundance of beneficial bacteria (, and ) and decreasing that of harmful bacteria ( and ). Meanwhile, the contents of short-chain fatty acids (SCFAs) increased. In conclusion, JM1 could alleviate intestinal barrier damage in colitis mice by modulating the tight junction structures, intestinal mucus layer, inflammatory cytokines, gut microbiota, and SCFAs. It can be considered a potential preventive strategy to alleviate colitis injury.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9823819 | PMC |
http://dx.doi.org/10.3390/nu15010139 | DOI Listing |
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