NLRP3炎症小体参与脑缺血再灌注损伤的研究进展

Advance in NLRP3 inflammasome involved in cerebral ischemia-reperfusion injury

脑缺血再灌注损伤是指脑组织供血不足,恢复血流灌注后引发缺血组织活性氧(ROS)积累导致的进一步损伤。这一过程引发固有免疫应答并导致炎症级联反应。随着近年对脑缺血再灌注损伤机制的深入研究,Nod样受体蛋白3(NLRP3)作为一种重要的模式识别受体,被发现参与了脑缺血再灌注的炎症损伤过程。而NLRP3炎症小体具有错综复杂的基础机制,尚未完全阐明。本文就NLRP3炎症小体结构、在脑缺血再灌注中的功能及基于NLRP3炎症小体衍生的潜在治疗方法进行综述。

Cerebral ischemia-reperfusion injury is further damage caused by accumulation of reactive oxygen species(ROS)in ischemic cerebral tissues after cerebrovascular blood supply is restored.This process triggers an innate immune response and leads to an inflammatory cascade.In recent years,with in-depth study of mechanism of cerebral ischemia-reperfusion injury,Nod-like receptor protein 3(NLRP3),an important pattern recognition receptor,has been found to participate in inflammatory injury process of cerebral ischemia-reperfusion.NLRP3 inflammasome has intricate underlying mechanisms that have not yet been fully understood.This article reviews structure of NLRP3 inflammasome and its function in cerebral ischemia-reperfusion,as well as potential treatments based on NLRP3 inflammasome.