Paeoniflorin protects NOD mice from T1D through regulating gut microbiota and TLR4 mediated myD88/TRIF pathway

特里夫 生物 TLR4型 点头 腹腔注射 点头老鼠 流式细胞术 免疫系统 免疫学 药理学 内分泌学 先天免疫系统 Toll样受体 糖尿病
作者
Cheng Luo,Danyi Yang,Can Hou,Tingting Tan,Chao Chen
出处
期刊:Experimental Cell Research [Elsevier BV]
卷期号:422 (1): 113429-113429 被引量:6
标识
DOI:10.1016/j.yexcr.2022.113429
摘要

This study aimed to explore the effect of PF in regulating the progression of T1D through regulating gut microbiota and inhibiting TLR4-myD88/TRIF pathway. T1D mouse models were established and received PF treatment through intraperitoneal injection. The glucose, sugar tolerance, the incidence of T1D and H&E staining were detected to verify the effect of PF on T1D. Meanwhile, the changes of gut microbiota and the permeability of intestines in mice were also measured. On parallel, the number and function of immune cells were detected by Flow Cytometry. The expressions of ZO-1, ZO-2 and TLR4-myD88/TRIF pathway related proteins were detected by western blotting. Mice received PF treatment had decreased incidence of T1D and inflammatory infiltration in islet tissues compared with those received PBS treatment. In addition to that, PF treated mice had increased Sutterella species and decreased intestinal permeability, in which the decreased ratio of Th1/Th17 and increased Treg cells were also identified. The expression of TLR4-myD88/TRIF pathway was also suppressed in response to PF treatment. Moreover, further treatment with TLR4 agonist, LPS, could reverse the effect of PF on T1D mice. PF can suppress the TLR4 mediated myD88/TRIF pathway to change the distribution of gut microbiota, so as to protect NOD mice from T1D.
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