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- W3100477206 abstract "• NK relieved DSS-induced chronic colitis. • NK maintained mucosal integrity by inhibiting apoptosis. • NK regulated gut microbiota of DSS-induced chronic colitis. • NK suppressed Trp metabolism via inhibiting IDO-1 in DSS-induced chronic colitis. In this study, we investigated the protective effect of Nattokinase (NK), the most active ingredient in natto used for healthcare, on dextran sulfate sodium (DSS)-induced chronic colitis and unraveled the potential mechanisms. NK dramatically attenuated clinical symptoms and pathological damage of DSS-induced chronic colitis. NK also inhibited proinflammatory cytokines production in DSS-induced colonic tissues. Mucosal integrity was maintained by NK. Moreover, nattokinase reversed DSS-induced decline of bacteria community diversity and intestinal microbial imbalance by decreasing levels of Firmicutes and increasing levels of Bacteroidetes . Tryptophan (Trp) metabolism analysis demonstrated that NK suppressed Trp catabolism especially the Kynurenine (Kyn) pathway in chronic colitis. Furthermore, NK strikingly down-regulated the protein expression of IDO-1 in chronic colitis mice. Taken together, the study demonstrated that NK relieved DSS-induced chronic colitis by regulating gut microbiota and suppressing Trp metabolism via inhibiting IDO-1. This study indicated that NK might be a promising and effective agent for IBD." @default.
- W3100477206 created "2020-11-23" @default.
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- W3100477206 date "2020-12-01" @default.
- W3100477206 modified "2023-09-23" @default.
- W3100477206 title "Nattokinase mitigated dextran sulfate sodium-induced chronic colitis by regulating microbiota and suppressing tryptophan metabolism via inhibiting IDO-1" @default.
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- W3100477206 doi "https://doi.org/10.1016/j.jff.2020.104251" @default.
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