炎症小体在缺血性脑卒中中的激活和作用机制的研究进展

Research Progress on the Activation and Mechanism of Action of Inflammasomes in Ischemic Stroke

缺血性脑卒中是临床常见的心血管疾病之一,致死率及致残率均较高。核苷酸结合寡聚化结构域样受体蛋白(NLRP)1、NLRP3、黑色素瘤缺乏因子2等炎症小体是缺血性脑卒中炎症反应的重要机制。而钾离子外流、活性氧过量产生以及缺氧诱导因子-1α信号通路和胱天蛋白酶1信号通路激活等是炎症小体激活的主要机制,并在缺血性脑卒中中通过炎症和(或)凋亡过程引发细胞死亡,发挥神经保护作用。因此,深入研究NLRP3等炎症小体引发缺血性脑卒中及炎症反应的相关机制,可以为疾病的抗炎治疗提供可靠依据。

Ischemic stroke is one of common clinical cardiovascular diseases with high mortality and morbidity.Inflammasomes such as nucleotide-binding oligomerization domain-like receptor protein(NLRP)1,NLRP3 and absent in melanoma 2 are important mechanisms of inflammatory response in ischemic stroke.And overproduction of potassium outflow,reactive oxygen species,and activation of hypoxia induced factor-1αsignaling pathway and caspase-1 signaling pathway are the main mechanisms of activation of inflammasomes,and cause cell death in the ischemic stroke by inflammation and/or apoptosis process,thus playing a role of protecting nerve.Therefore,in-depth research on the mechanisms by which inflammasomes such as NLRP3 trigger ischemic stroke and inflammatory responses can provide reliable evidence for anti-inflammatory treatment of the disease.