结肠炎
巨噬细胞极化
炎症体
体内
脂多糖
化学
NF-κB
免疫系统
信号转导
癌症研究
肿瘤坏死因子α
细胞生物学
体外
药理学
免疫学
巨噬细胞
炎症
医学
生物
生物化学
生物技术
作者
Hao-yue Zhang,Hairong Zeng,Huizhen Wei,Xia-Yan Chu,Honghao Zhu,Bin Zhao,Yang Zhang
出处
期刊:Phytomedicine
[Elsevier]
日期:2022-12-01
卷期号:107: 154455-154455
被引量:5
标识
DOI:10.1016/j.phymed.2022.154455
摘要
Macrophages infiltration and activation play multiple roles in maintaining intestinal homeostasis and participate in the occurrence and development of UC. Thus, the restoration of immune balance can be achieved by targeting macrophage polarization. Previous studies have reported that TXYF could effectively ameliorate DSS-induced colitis. However, the underlying mechanisms of TXYF for DSS-induced colitis are still ill-defined.This study was designed to explore the therapeutic effect of TXYF and its regulation in macrophages polarization during DSS-induced mice. In C75BL/6 mice, dextran sulfate sodium (DSS) was used to induce colitis and concomitantly TXYF was taken orally to evaluate its curative effect. In vitro experiment was implemented on BMDMs by lipopolysaccharide, IFN- and ATP.Here, we found that TXYF ameliorated clinical features in DSS-induced mice, decreased macrophages M1 polarization but remarkably increased M2 polarization. Mechanically, TXYF treatment effectively inhibited the activities of nuclear transcription factor NF-κB, which further contributed to the decrease of the inflammasome genes of NLRP3, limiting the activation of NLRP3 inflammasome in vivo and in vitro.Our findings demonstrated administration of TXYF can interfere with macrophage infiltration and polarization to improve the symptoms of acute colitis, by repressing NF-κB/NLRP3 signaling pathway activation. This enriches the mechanism and provides new prospect for TXYF in the treatment of colitis.
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