Nrf2通过调节巨噬细胞极化治疗溃疡性结肠炎的机制

Mechanism of Nrf2 in the treatment of ulcerative colitis via regulating macrophage polarization.

作者信息

Zhang Yilin, Liu Yushan, Yang Shusen, Yan Shuguang

机构信息

Basic Medical College, Shaanxi University of Chinese Medicine, Xianyang Shaanxi 712046.

Key Laboratory of Prescriptions and Medicines for Gastrointestinal Diseases in Shaanxi Province, Xianyang Shaanxi 712046, China.

出版信息

Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2023 Nov 28;48(11):1746-1752. doi: 10.11817/j.issn.1672-7347.2023.230281.

Abstract

Ulcerative colitis (UC) is an inflammatory bowel disease induced by multiple factors, which causes abnormal activation of intestinal immune cells and excessive release of antibodies and inflammatory factors, repeatedly damaging the intestinal mucosa. Macrophages, as innate intestinal immune cells, often maintain the balance of M1/M2 macrophages polarization to normalize the regression inflammation, and the imbalance of their polarization will cause repeated damage of intestinal mucosa and persistent inflammation, which is a main cause of UC. Nuclear factor E2-related factor 2 (Nrf2), as an important regulator of antioxidant and anti-inflammatory, is often used as a target for the treatment of autoimmune diseases.Nrf2 alleviates intestinal high oxidative stress and inflammatory factors by balancing macrophage polarization, which may be of great significance for the prevention and treatment of UC. Summarizing the mechanism of macrophage polarization imbalance on the course of UC and the possible regulatory mechanism of Nrf2 may provide basis for the development of UC targeted therapeutic drugs.

摘要

溃疡性结肠炎(UC)是一种由多种因素诱发的炎症性肠病,它会导致肠道免疫细胞异常激活以及抗体和炎症因子过度释放,反复损伤肠黏膜。巨噬细胞作为肠道固有免疫细胞,常维持M1/M2巨噬细胞极化平衡以使炎症消退正常化,其极化失衡会导致肠黏膜反复损伤和炎症持续存在,这是UC的主要病因之一。核因子E2相关因子2(Nrf2)作为抗氧化和抗炎的重要调节因子,常被用作自身免疫性疾病的治疗靶点。Nrf2通过平衡巨噬细胞极化减轻肠道高氧化应激和炎症因子,这可能对UC的防治具有重要意义。总结巨噬细胞极化失衡在UC病程中的机制以及Nrf2可能的调控机制,可为UC靶向治疗药物的研发提供依据。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索