NLRP3炎性小体在缺氧性肠道应激致肺损伤中的作用及机制  

Role of NLRP3 inflammasomes in lung injury induced by gut hypoxic stress and its mechanism

作　　者：熊诗强[1] 周其全[1] 

机构地区：[1]第三军医大学高原军事医学系高原疾病教研室高原医学教育部重点实验室全军高原医学重点实验室,重庆400038

出　　处：《解放军医学杂志》2014年第11期912-917,共6页Medical Journal of Chinese People's Liberation Army

基　　金：国家科技支撑计划课题(2009BAI85B03);军队“十一五”攻关课题(08G093)~~

摘　　要：肠道发生缺氧性应激时,肠黏膜屏障功能受损,肠源性损伤物质可移位至肠外空间,导致远隔脏器出现功能障碍,尤其是可导致急性肺损伤(ALI)的发生。高原肺水肿(HAPE)是由高原缺氧引起的非心源性肺损伤,炎症因素参与HAPE的发生已逐渐得到认同,而NLRP3炎性小体介导的促炎因子分泌在肺损伤的发生中起重要作用。缺氧性肠道应激和NLRP3炎性小体可能参与了HAPE的发生发展。探讨NLRP3炎性小体在缺氧性肠道应激致肺损伤中的作用及机制,对指导缺氧性炎症疾病的治疗具有重要临床意义。Hypoxic stress of the gut may induce impairment of gut barrier function,ensuing translocation of gutderived factors which can damage the function of remote organs,especially the development of acute lung injury（ALI）.High altitude pulmonary edema（HAPE） is a non-cardiogenic pulmonary injury caused by hypoxia,while inflammation involved in the pathogenesis of HAPE has been gradually recognized.It has been also recognized that the cleavage and maturation of proinflammatory cytokines mediated by NLRP3 inflammasome play a crucial role in the pathogenesis of lung injury.Further investigation on the role of NLRP3 inflammasome in lung injury induced by gut hypoxic stress is of an important clinical significance for further improvement in the treatment of hypoxic inflammatory diseases.

关 键 词：胃肠疾病 缺氧 应激 NLRP3炎性小体 肺损伤 

分 类 号：R574[医药卫生—消化系统] R563[医药卫生—内科学]