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Chinese Journal of Biochemistry and Molecular Biology ; (12): 749-761, 2022.
Article in Chinese | WPRIM | ID: wpr-1015690

ABSTRACT

n-3 polyunsaturated fatty acids (PUFAs) play an active role in controlling the progression of ulcerative colitis (UC), but its mechanism is not very clear. In this study, we compared the effects of fish oil (the main component is n-3 PUFAs) in the mouse model with acute and chronic colitis induced by dextran sulfate sodium (DSS). Male C57BL/6J mice were randomly divided into six groups, and each group had ten mice. The alleviating effect of fish oil on chronic colitis was significantly better than acute colitis as indicated by the following analysis: the weight loss of mice (P < 0. 05), decreased disease activity index (DAI) score (P<0. 05), colonic edema, colon length index and histopathological score (P < 0. 05), and serum pro-inflammatory factor levels like IL-1β, TNF-α, and IL-6 (P < 0. 01). Moreover, fish oil promoted the level of serum anti-inflammatory factor IL-10 (P<0. 05). The treatment of fish oil increased the n-3 PUFA concentration in the intestinal epithelium of mice (P < 0. 01), especially EPA (P<0. 05). 16S rRNA sequencing of feces revealed that fish oil significantly increased the relative abundance of butyrate-producing flora (Clostridiales) and probiotics (Bifidobacteriales) in the feces of the maintained remission model group, reduce the proportion of aerobic, parthenogenic anaerobic and pathogenic, and improved the disorder of glycan biosynthesis and metabolism and oxidative phosphorylation (P<0. 05). Compared with the induced remission fish oil group, fish oil treatment led to an elevated expression of mechanical barrier and energy metabolism pathway proteins in the maintained remission fish oil group. Our results showed that fish oil exerted a more potent inhibitory effect in the remission mice model, which may be related to effectively strengthening the mechanical barrier, improving the composition and function of intestinal microbiota and concentration of butyric acids and improving dysbiosis of host-microbial interaction.

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