肠道菌群
Treg细胞
小檗碱
溃疡性结肠炎
结肠炎
医学
平衡(能力)
免疫学
失调
内科学
药理学
免疫系统
疾病
T细胞
白细胞介素2受体
物理医学与康复
作者
Huantian Cui,Yimei Cai,Li Wang,Beitian Jia,Junchen Li,Shuwu Zhao,Xiaoqian Chu,Jin Lin,Xiaoyu Zhang,Yuhong Bian,Pengwei Zhuang
标识
DOI:10.3389/fphar.2018.00571
摘要
Berberine (BBR), an alkaloid isolated from Rhizoma Coptidis, Cortex Phellode, and Berberis, has been widely used in the treatment of ulcerative colitis (UC). However, the mechanism of BBR on UC is unknown. In this study, we investigated the activities of T regulatory cell (Treg) and T helper 17 cell (Th17) in a dextran sulfate sodium (DSS)-induced UC mouse model after BBR administration. We also investigated the changes of gut microbiota composition using 16S rRNA analysis. We also examined whether BBR could regulate the Treg/Th17 balance by modifying gut microbiota. The mechanism was further confirmed by depleting gut microbiota through a combination of antibiotic treatment and fecal transplantations. Results showed that BBR treatment could improve the Treg/Th17 balance in the DSS-induced UC model. BBR also reduced diversity of the gut microbiota and interfered with the relative abundance of Desulfovibrio, Eubacterium, and Bacteroides. Moreover, BBR treatment did not influence the Treg/Th17 balance after the depletion of gut microbiota. Our results also revealed that fecal transplantation from BBR-treated mice could relieve UC and regulate the Treg/Th17 balance. In conclusion, our study provides evidence that BBR prevents UC by modifying gut microbiota and regulating the balance of Treg/Th17.
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