失调
肠道菌群
牛磺去氧胆酸
生物
微生物学
结肠炎
免疫学
生物化学
未折叠蛋白反应
细胞凋亡
作者
Yuqi Wu,Yanfei Zheng,Xiaolu Wang,Ping Tang,Wenqian Guo,Han Ma,Anqi Zhang,Delong Li,Yuxin Xie,Chong‐Zhi Wang,Haiqiang Yao,Jin‐Yi Wan,Chun‐Su Yuan
标识
DOI:10.1142/s0192415x23500325
摘要
was negatively correlated with body weight and colon length, and positively correlated with disease activity index and IL-1[Formula: see text]. Furthermore, through gut microbiota depletion, we confirmed that SJZD exerted anti-inflammatory activities in a gut microbiota-dependent manner, and fecal microbiota transplantation (FMT) validated the mediating role of gut microbiota in the SJZD treatment of UC. Through gut microbiota, SJZD modulates the biosynthesis of bile acids (BAs), especially tauroursodeoxycholic acid (TUDCA), which has been identified as the signature BA during SJZD treatment. Cumulatively, our findings disclose that SJZD attenuates UC via orchestrating gut homeostasis in microbial modulation and intestinal barrier integrity, thus offering a promising alternative approach to the clinical management of UC.
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