ROS与脓毒症NLRP3活化的关系及其调控机制  

Correlation of reactive oxygen species with NLRP3 inflammasome activation in sepsis and its mechanisms

作　　者：韩雪妹(综述) 王日兴(审校)[1] HAN Xue-mei;WANG Ri-xing(Department of Emergency,the Second Affiliated Hospital of Hainan Medical University,Haikou 570311,Hainan,CHINA)

机构地区：[1]海南医学院第二附属医院急诊科,海南海口570311

出　　处：《海南医学》2022年第14期1871-1874,共4页Hainan Medical Journal

基　　金：海南省自然科学基金(编号:818MS148)。

摘　　要：NLRP3是目前研究最为广泛的炎性体之一,并且是固有免疫的关键组分之一。在各种内外源性刺激因素作用下,核心蛋白NLRP3、连接蛋白ASC以及效应蛋白pro-caspase-1在胞质内组装成为NLRP3炎性体,形成具有催化活性的Caspase-1,后者将pro-IL-1β、pro-IL-18剪切成IL-1β、IL-18并分泌至效应部位参与炎症反应的发生、发展过程。过度活化的NLRP3炎性体可致机体内产生过度的炎症反应,是导致脓毒症和多器官功能障碍的重要原因。目前对NLRP3炎性体活化的具体调控机制研究仍不完全,但是众多的研究表明,其激活的关键因素之一是活性氧(ROS)的产生。本文将着眼于探讨ROS在调控脓毒症NLRP3炎性体活化中的作用研究。Nucleotide-binding domain and leucine-rich repeat protein-3(NLRP3)inflammasome is one of the most widely studied inflammasome and one of the key components of innate immunity.Under the action of various exogenous stimulus factors,the core protein NLRP3,apoptosis-like protein containing a caspase recruitment domain(ASC),and the cysteine aspartate specific protease-1 precursor(pro-caspase-1)are assembled into NLRP3 inflammasome in cytoplasm,forming catalytic caspase-1,which cleaves interleukin 1βprecursor(pro-IL-1β)and interleukin 18 precursor(pro-IL-18)into interleukin 1β(IL-1β)and interleukin 18(IL-18).Excessive activation of NLRP3 inflammasome can cause excessive inflammatory reaction in the body,which is an important cause of sepsis and multiple organ dysfunction.At present,the research on the specific regulatory mechanism of NLRP3 inflammasome activation is still incomplete,but many studies have shown that one of the key factors of NLRP3 activation is the production of reactive oxygen species(ROS).This article will focus on the role of ROS in regulating the activation of NLRP3 inflammasome in sepsis.

关 键 词：脓毒症 炎性体 NLRP3炎性体 活性氧 线粒体 

分 类 号：R631[医药卫生—外科学]