炎性小体在急性胰腺炎发病机制中的研究进展

Research progresses of inflammasome in the pathogenesis of acute pancreatitis

急性胰腺炎(AP)是临床常见急症,腺泡细胞的死亡导致的无菌炎症是AP的早期病理学变化,但随后发生过度炎症反应导致多器官功能障碍是病情加重的主要机制。其中,炎性小体的组装激活参与介导了这一发病过程。炎性小体激活的代谢调节以及所产生的调节效应物对AP及其炎症反应机制起重要决定因素。文章主要从炎性小体的结构与功能及其在AP发病机制中的作用进行综述。

Acute pancreatitis(AP)is a common clinical emergency. Aseptic inflammation caused by the death of acinar cells is the early pathological change of AP. However,the main mechanism of aggravation of AP is the subsequently excessive inflammation which leads to multiple organ dysfunctions. Among them,the assembly and activation of inflammatory corpuscles are involved in the pathogenesis. It has shown that metabolic regulation of inflammatory corpuscle activation and its regulatory effectors play an important and decisive role in AP and its inflammatory response mechanism. This article reviews the structure and function of inflammasomes and their role in the pathogenesis of AP.