炎性小体在脑梗死病程中的作用  

The role of inflammasome in cerebral infarction

作　　者：王兆鑫 张文静[1] 查才军 刘彦虹[1] Wang Zhaoxin;Zhang Wenjing;Zha Caijun;Liu Yanhong(Department of Clinical Laboratory,the Second Affiliated Hospital of Harbin Medical University,Harbin 150086,China)

机构地区：[1]哈尔滨医科大学附属第二医院检验科,150086

出　　处：《国际免疫学杂志》2019年第3期324-328,共5页International Journal of Immunology

摘　　要：脑梗死(cerebral infarction,CI)是一种高致残及致死率的缺血性脑血管疾病,炎症反应在其发生和发展中起到了关键的作用。炎性小体是由胞浆内模式识别受体(pattern recognition receptor,PRRs)参与装配的多蛋白复合物,是固有免疫系统的重要组成部分之一。脑梗死的炎症反应由多种分子通过复杂途径进行调节,炎性小体在其中扮演重要角色。炎性小体和白细胞介素(interleukin,IL)-1可随细胞死亡释放到胞外,发挥传递炎症信号和引发炎症反应的作用,因此有必要就炎性小体在脑梗死病程中的作用进行总结与分析。Cerebral infarction(CI)is a cerebrovascular disease with high disability and mortality.Inflammatory reaction plays a key role in the development of CI.The most principal part in inflammation process is inflammasome,which is regulated by a variety of molecules through complex pathways in CI.Inflammasome,a protein complexes assembled by pattern recognition receptors(PRRs)in the cytoplasm,is the important component of innate immune system.PRRs recruit and activate caspase-1,an inflammatory protease,through pathogen-associated molecular patterns(PAMPs)or the hos-derived damage associated molecular patterns(DAMPs)recognition reaction.Activated caspase-1 induces specific cell death under inflammatory conditions by regulating caspase-1-dependent pyroptosis.Interleukin 1(IL-1)is released to extracellular matrix and triggers inflammation and cell death.Here we review and analyze the role of inflammasome in the course of cerebral infarction.

关 键 词：脑梗死 炎性小体 炎症反应 白细胞介素-1 胱冬肽酶-1 细胞焦亡 

分 类 号：R743.3[医药卫生—神经病学与精神病学]