Objective To investigate the effects of Nicotinamide mononucleotide (NMN) on ulcerative colitis induced by dextran sulfate sodium (DSS) in mice. Methods DSS-induced ulcerative colitis mice were used to evaluate the effects of NMN. After NMN administration, the survival time, weight, disease activity index (DAI), colon tissue length and pathological changes of colon tissue slices were observed. Results NMN did not cause significant changes in the survival time, weight, DAI, and intestinal morphology of ulcerative colitis mice. Conclusion NMN has no significant effect on DSS-induced ulcerative colitis mice.

Objective To investigate the effect of intestinal Metrnl on dextran sodium sulfate (DSS)-induced ulcerative colitis mouse model and the regulation mechanism of intestinal microbiota. Methods Different concentrations of DSS (3% DSS and 1% DSS) were used to induce ulcerative colitis on C57 mice to determine the experimental conditions. Intestinal epithelial Metrnl specific knockout mice (Metrnl^(-/-)) and its control mice (Metrnl^(+/+)) were administrated with 3% DSS for 5 d. Then the survival time, body weight, DAI (disease activity index), colon length and pathological changes in colon tissues were observed. 16S ribosomal RNA gene sequencing was used to detect the composition of intestinal microbiota. Results Compared with 1% DSS, 3% DSS could significantly aggravate ulcerative colitis on C57 mice, such as lower survival rate (P<0.05), more weight loss (P<0.05), higher DAI score (P<0.05), shorter colon length (P<0.05) and higher pathology score (P<0.05). After administrated to 3% DSS for 5 d, comparing with Metrnl^(+/+) mice, Metrnl^(-/-) mice showed more weight loss (P<0.05), higher DAI score (P<0.05), shorter colon length (P<0.05) and higher pathology score (P<0.05). The 16S ribosomal RNA results showed that the diversity of intestinal microbiota in Metrnl^(-/-) mice significantly decreased. Furthermore, Bacteroidetes and Proteobacteria significantly decreased, while Firmicutes increased. Conclusion Metrnl could protect the DSS-induced ulcerative colitis mouse through regulating intestinal microbiota.