Nattokinase mitigated dextran sulfate sodium-induced chronic colitis by regulating microbiota and suppressing tryptophan metabolism via inhibiting IDO-1. (December 2020)

• Record Type: Journal Article
• Authors: Zhou, Lvqi; Hao, Ning; Li, Xiaotian; Chen, Jiaxi; Yang, Runyu; Song, Changqin; Sun, Yang; Zhang, Qi
• Is Part Of: Journal of functional foods. Volume 75(2020)
• Publication Date: 2020-12
• Subjects: Nattokinase (NK) -- Chronic colitis -- Gut microbiota -- Tryptophan metabolism -- Indoleamine 2 -- 3-dioxygenase 1 (IDO-1); Functional foods -- Analysis -- Periodicals; Food -- Biotechnology -- Periodicals; Nutrition -- Periodicals; 613.2
• DOI: 10.1016/j.jff.2020.104251
• Languages: English
• ISSNs: 1756-4646

Abstract

Graphical abstract: Highlights: 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. Abstract: 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.