PI3K/AKT/mTOR通路
蛋白激酶B
FOXP3型
促炎细胞因子
信号转导
结肠炎
免疫学
溃疡性结肠炎
流式细胞术
医学
癌症研究
生物
免疫系统
细胞生物学
炎症
内科学
疾病
作者
Baosen Zhou,Fuchun Liu,Hai-Mei Zhao,Xiaoyun Zhang,Haiyan Wang,Duan‐Yong Liu
标识
DOI:10.1016/j.jep.2020.113211
摘要
As a classic prescription and commercial Chinese patent medicine, Zuojin Pill (ZJP) has been used to treat ulcerative colitis (UC) effectively for many years. However, its mechanism of action remains unclear. Aim of the study: Mice with dextran-sulfate-sodium-induced colitis were treated with ZJP for 7 d. In the present study, the therapeutic effect of ZJP was evaluated by macroscopic and microscopic observation; regulatory T (Treg) cells and their subsets were analyzed by flow cytometry; and the composition of gut microbiota was tested by 16S rRNA analysis. Activation of the phosphoinostide 3-kinase (PI3K)/Akt signaling pathway was observed by western blotting. The pathological damage was attenuated and expression of proinflammatory cytokines was decreased. While the diversity of intestinal microflora was regulated, the relative abundance of Actinobacteria, and Sphingobacteriia was modified. Meanwhile, the level of CD4+CD25+Foxp3+ and PD-L1+ Treg cells improved. These changes maintained a positive correlation which was analyzed statistically. Our results also showed that ZJP inhibited activation of the PI3K/Akt signaling pathway. ZJP regulates crosstalk between intestinal microflora and Treg cells to attenuate experimental colitis via the PI3K/Akt signaling pathway.
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