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.
溃疡性结肠炎(ulcerative colitis，UC)是由多因素诱导，致使肠道免疫细胞被异常激活并过量释放炎症因子，反复损伤肠道黏膜的一种炎症性肠病。巨噬细胞作为肠道固有免疫细胞，常通过维持M1/M2型巨噬细胞极化的平衡使炎症正常转归。而其极化的失衡会造成肠黏膜反复受损、炎症迁延不愈，是引发UC的重要因素。核因子E2相关因子2(nuclear factor E2-related factor 2，Nrf2)作为抗氧化、抗炎的重要调节器，常作为治疗自身免疫性疾病的靶点。Nrf2通过平衡巨噬细胞极化进而缓解肠道高氧化应激和炎症因子状态，对防治UC具有重要意义。总结巨噬细胞极化失衡在UC病程中的作用机制及Nrf2的调节机制，可为UC靶向治疗药物的开发提供参考。.
Keywords: macrophage polarization; nuclear factor E2-related factor 2; oxidative stress; ulcerative colitis.