Nod样受体蛋白3炎性小体在脑缺血再灌注损伤中的研究现状 Advance in Nod-like Receptor Protein 3 Inflammasome in Cerebral Ischemia Reperfusion Injury

Abstract

【摘要】 缺血再灌注损伤作为缺血性卒中的主要病理生理过程，能够引发固有免疫应答，导致无菌性炎症。越来越多的研究表明，固有免疫在脑缺血再灌注损伤中发挥着重要的作用，其中Nod样受体蛋白3（nod-like receptor protein 3，NLRP3）作为模式识别受体能够在机体受到损伤时识别损伤相关分子模式，形成炎性小体，引发炎症因子趋化及炎性损伤。本文对NLRP3炎性小体的结构、功能、信号通路及其在脑缺血再灌注损伤中作用的研究进展进行介绍。 【Abstract】 Ischemia reperfusion injury after recanalization in ischemic stroke can trigger innate immune reaction, which can cause aseptic inflammation. More and more studies revealed that innate immune response played a critical role in ischemia reperfusion injury. When injure occurs, nod-like receptor protein 3 (NLRP3) inflammasome, a pattern recognition receptor, can be directly activated via external pathological signals known as pathogen-associated molecular patterns and endogenous damage-associated molecular patterns, which can activate intracellular innate immune receptors and cause immune reaction. This article reviewed the structure, function and signal pathways of NLRP3 inflammasome, and pathological mechanism of NLRP3 in ischemia reperfusion injury.

Keywords

• nod样受体蛋白3
• 缺血再灌注
• 炎性小体
• nod-like receptor protein
• ischemia reperfusion
• inflammasome