NLRP3炎性小体在急性胰腺炎发病机制中的研究进展  

Research Progress of NLRP3 Inflammasome in Pathogenesis of Acute Pancreatitis

作　　者：李昂嫣 孙元佳 张楚悦 艾迎春[1] Li Angyan;Sun Yuanjia;Zhang Chuyue;Ai Yingchun(The First Affiliated Hospital of Jiamusi University,Jiamusi 154000,China)

机构地区：[1]佳木斯大学附属第一医院,黑龙江佳木斯154000

出　　处：《广东化工》2021年第3期145-146,144,共3页Guangdong Chemical Industry

摘　　要：急性胰腺炎(AP)是临床常见的急腹症之一,是一种由多种病因引起胰腺组织自身消化所导致的复杂性炎症性疾病,局部的无菌性炎症是该疾病最初的主要表现形式,随着疾病的发展,引起全身性炎症反应综合征,该反应可引起严重的多器官衰竭,成为该疾病死亡的主要原因。近几年,随着对急性胰腺炎发病机制的深入研究,国内外研究者发现,炎性小体的激活及其代谢调控因子在AP的发病机制中起了关键作用。本文主要探讨NLRP3炎性小体及其与急性胰腺炎病情发展的关系。Acute pancreatitis(AP)is one of the most common acute abdomen in clinical practice.It is a complex inflammatory disease caused by the digestion of pancreatic tissue caused by various causes.In the early stage of the disease,local aseptic inflammation is the main cause of systemic inflammatory response syndrome,which can cause severe multiple organ failure and become the main cause of death of the disease.In recent years,with the in-depth study on the pathogenesis of acute pancreatitis,studies at home and abroad have found that the activation of inflammatory corpuscles and their metabolic regulatory effectors play a key role in the pathogenesis of AP.This paper mainly discusses the relationship between NLRP3 inflammatory corpuscles and the development of acute pancreatitis.

关 键 词：急性胰腺炎 炎性小体 NLRP3 

分 类 号：TQ[化学工程]