基于Notch/NF-κB/NLRP3信号通路的巨噬细胞活化与溃疡性结肠炎的研究进展

溃疡性结肠炎是一种以腹泻、腹痛、脓血便为主要表现的肠道免疫炎症性疾病，由巨噬细胞超活化所导致的非可控性炎症是溃疡性结肠炎发病和逐渐恶化的重要原因，因此抑制巨噬细胞超活化是治疗溃疡性结肠炎的有效途径之一。Notch信号通路参与了调节巨噬细胞的免疫应答并促进炎症反应，NF-κB信号通路是参与炎症反应的“明星通路”，NLRP3炎症小体参与了巨噬细胞的活化过程，在已有的免疫炎症性疾病中Notch，NF-κB，NLRP3炎症小体三者之间构成了上下游的信号转导通路，Notch可通过NF-κB/NLRP3炎症小体信号通路调节巨噬细胞的活化。

Progress in the study of macrophage activation and ulcerative colitis from the Notch/NF-κB/NLRP3 signaling pathway

Ulcerative colitis is an intestinal infl ammatory disease characterized by diarrhea, abdominal pain andpurulent stool. Uncontrolled infl ammation caused by macrophage hyper-activation is an importantcause of ulcerative colitis. Th erefore, inhibiting macrophage hyper-activation is an eff ective way totreat ulcerative colitis. Notch signaling pathway is involved in regulating the immune response ofmacrophages and promoting inflammation. NF-κB signaling pathway is the “star pathway” involvedin inflammation. NLRP3 inflammatory body is involved in the activation of macrophages. Notch,NF-κB and NLRP3 inflammatory bodies constitute the upstream and downstream signal pathwaysin the existing immune inflammatory diseases. Notch signal pathway can regulate the activation ofmacrophage via NF-κB/NLRP3 inflammatory body signaling pathway.