NLRP3炎症小体在动脉粥样硬化中的作用研究进展  

Research progress on the role of NLRP3 inflammasome in atherosclerosis

作　　者：解静[1] 程琦 刘昳佳 高杉[1] 于春泉[1] XIE Jing;CHENG Qi;LIU Yijia;GAO Shan;YU Chunquan(Tianjin University of Traditional Chinese Medicine,Tianjin 301617,China)

机构地区：[1]天津中医药大学,天津301617

出　　处：《天津中医药》2020年第4期469-474,共6页Tianjin Journal of Traditional Chinese Medicine

基　　金：国家自然科学基金项目(81403198);国家重点基础研究发展计划(973计划)项目(2014CB542902)。

摘　　要：NOD样受体热蛋白结构域3(NLRP3)炎症小体是核酸结合的寡聚化结构域样受体(NLR)炎性通路中的重要组成部分,由NLRP3支架、凋亡相关斑点样蛋白(ASC)和含半胱氨酸的天冬氨酸蛋白水解酶-1前体(pro-Caspase-1)组成,激活的NLRP3炎症小体通过促进含半胱氨酸的天冬氨酸蛋白水解酶-1(Caspase-1)、白细胞介素-1β(IL-1β)、白细胞介素-18(IL-18)等关键下游细胞因子的产生和分泌,增强炎症反应,以维持机体的固有免疫和特异性免疫。研究显示,NLRP3炎症小体可影响动脉粥样硬化、免疫性疾病、炎症性疾病等多种类型疾病的进程,是目前研究最为广泛的炎性小体,已成为近年来的研究热点。文章从炎症反应机制角度出发,主要探讨NLRP3炎症小体的激活对动脉粥样硬化的调控作用。Nod-like receptor protein 3(NLRP3)inflammasome is an important component of NLR inflammatory pathway,which is composed of NLRP3 scaffold,ASC(apoptosis-associated speck-like protein containing CARD)and pro-Caspase-1.The activated NLRP3 inflammasome can enhance the inflammatory response by promoting the production and secretion of key downstream cytokines,such as Caspase-1,interleukin-1β(IL-1β),IL-18(interleukin-18),and so on.Thus,the inherent immunity and specific immunity of the body could be maintained.Studies have shown that NLRP3 inflammasome,as the most widely studied inflammasome and the cytokines that can affect the progress of atherosclerosis,immune diseases,inflammatory diseases and other types of diseases,has become a research hotspot in recent years.This article mainly discusses the regulatory effect of the activated NLRP3 inflammasome in atherosclerosis from the mechanisms of inflammatory response.

关 键 词：NLRP3炎症小体 炎症反应 动脉粥样硬化 冠状动脉粥样硬化 颅内动脉粥样硬化 糖尿病 

分 类 号：R392[医药卫生—免疫学]