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Blautia producta displays potential probiotic properties against dextran sulfate sodium-induced colitis in mice

Food Science and Human Wellness 2024年第2期13卷 709-720页

作者： Bingyong Mao Weiling Guo Shumao Cui Qiuxiang Zhang Jianxin Zhao Xin Tang Hao Zhang State Key Laboratory of Food Science and Resources Jiangnan UniversityWuxi 214122China School of Food Science and Technology Jiangnan UniversityWuxi 214122China National Engineering Research Center for Functional Food Jiangnan UniversityWuxi 214122China

Blautia has attracted attention because of its potential efficacy in ameliorating host energy metabolism and *** study aims to investigate the influences of Blautia producta D4 on colitis induced by dextran sulfate sodium(DSS)and to reveal the underlying *** showed that *** D4 intervention significantly relieved body weight loss,and suppressed the elevation of pro-inflammatory cytokines(including interleukin-6(IL-6),tumor necrosis factor-α(TNF-α),and interleukin-1β(IL-1β))and excessive oxidative stress(myeloperoxidease(MPO)activity,superoxide dismutase(SOD)activity,glutathione peroxidase(GSH-Px)activity,and malondialdehyde(MDA)level)in colitis ***,the concentrations of tight junction proteins(occludin,claudin-1,and ZO-1)related to the intestinal barrier were obviously elevated,and colitis-related TLR4/NF-κB pathway activation was remarkably inhibited after *** D4 *** intestinal microbial disorder was evidently ameliorated by increasing the relative abundance of Clostridium sensu stricto 1,Bifidobacterium,GCA-900066225,Enterorhabdus,and reducing the relative abundance of Lachnospiraceae NK4A136 *** conclusion,oral administration of *** D4 could ameliorate DSS-induced colitis by suppressing inflammatory responses,maintaining the intestinal barrier,inhibiting TLR4/NF-κB pathway,and regulating intestinal microbiota *** results are conducive to accelerate the development of *** D4 as a functional probiotic for colitis.

关键词： Blautia producta D4 Colitis intestinal mechanical barrier TLR4/NF-κB pathway intestinal microbiot

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