摘要
急性胰腺炎是胰酶提前激活造成的胰腺以及周围组织自身消化的一种急性炎症,胰腺腺泡细胞内胰蛋白酶原提前激活和炎症反应的级联效应被认为是导致急性胰腺炎发生、发展的关键机制.而自噬作为Ⅱ型程序性死亡,出现在急性胰腺炎的早期病理过程中,其自噬通路受阻可加重胰腺炎时腺泡细胞的坏死程度.本文主要就自噬的最新研究进展及其在急性胰腺炎发生发展机制中的作用作一综述.
Acute pancreatitis （AP） is activated trypsin-induced pancreatic and its peripheral tissue inflammation caused by their own digestion.The activation in advance of trypsinogen and the inflammation cascade in pancreatic acinar cells are thought to be a key mechanism of the onset and development of AP.Autophagy pathway acting as Ⅱ type of programmed cell death occurs in the early pathological course of AP,blockade of which contributes to aggravating necrosis of acinar cells in AP.This article mainly discussed the recent advances in the understanding of autophagy researches and its function in the mechanism of AP.
出处
《国际外科学杂志》
2015年第6期417-421,共5页
International Journal of Surgery
关键词
胰腺炎
自噬
胰蛋白酶原
Pancreatitis
Autophagy
Trypsinogen
