NLRP3炎症小体及其在肝脏缺血-再灌注损伤中的作用机制  

NLRP3 inflammasome and its mechanism in liver ischemia-reperfusion injury

作　　者：张云飞 吐尔洪江·吐逊 Zhang Yunfei;Tuerhongjiang·Tuxun(Department of Liver and Laparoscopic Surgery,the First Affiliated Hospital of Xinjiang Medical University,Urumqi 830054,China;State Key Laboratory of Pathogenesis,Prevention and Treatment of High Incidence Diseases in Central Asia,Xinjiang Medical University,Urumqi 830054,China)

机构地区：[1]新疆医科大学第一附属医院消化血管外科中心肝脏·腹腔镜外科,乌鲁木齐830054 [2]新疆医科大学省部共建中亚高发病成因与防治国家重点实验室,乌鲁木齐830054

出　　处：《中华肝脏外科手术学电子杂志》2024年第3期398-403,共6页Chinese Journal of Hepatic Surgery(Electronic Edition)

基　　金：国家自然科学基金(82260411,82270632);新疆维吾尔自治区科技厅重点实验室开放课题(2018D04002)。

摘　　要：肝脏缺血-再灌注损伤(IRI)是指肝脏组织缺血一段时间后血流重新恢复却导致肝脏组织损伤加重的现象。炎症反应是引起肝脏IRI的主要原因之一,其中NLRP3炎症小体受体介导的炎症反应占主导地位。研究表明,通过抑制炎症小体的激活可以改善IRI。这篇综述总结了NLRP3介导炎症小体激活及调控的最新进展,以及它在肝脏IRI中的作用机制。Liver ischemia-reperfusion injury (IRI) refers to the restoration of oxygenated blood flow to the liver after a period of liver ischemia,which exacerbates liver injury.Inflammatory reaction is one of the main causes of liver IRI,and inflammatory reaction mediated by NLRP3 inflammasome receptor is dominant.Studies have shown that IRI can be alleviated by inhibiting the activation of inflammasomes.In this article,the latest progress in NLRP3-mediated activation and regulation of inflammasomes,and its mechanism in liver IRI were reviewed.

关 键 词：NLRP3 炎症小体 肝脏 缺血-再灌注损伤 

分 类 号：R657.3[医药卫生—外科学]