急性胰腺炎细胞凋亡机制研究进展  

Advance in acute pancreatitis apoptosis mechanisms

作　　者：石星亮[1] 陈垦[1] 王晖[2] 龙友明[1] 

机构地区：[1]广东药学院临床医学院内科学教研室,广东省广州市510310 [2]广东药学院中药学院药理学教研室,广东省广州市510006

出　　处：《世界华人消化杂志》2009年第6期594-597,共4页World Chinese Journal of Digestology

基　　金：广东省科学事业计划基金资助项目;No.2007B030702004;广州市科学技术基金资助项目;No.2007Z3-E5011;广东省自然科学基金资助项目;No.8151022401000012~~

摘　　要：急性胰腺炎(acute pancreatitis,AP)是临床上常见的危重疾病.该病的发病机制复杂,以往研究多集中在炎症因子、氧化应激、微循环障碍等方面.近年人们发现细胞凋亡在急性胰腺炎的发生发展过程中起重要作用,他参与了急性胰腺炎的组织损伤,但同时也是机体其中一种重要的自身保护机制.本文简述细胞凋亡与急性胰腺炎之间的关系,探讨细胞凋亡对急性胰腺炎器官损伤的影响,分析细胞凋亡与炎症因子、氧化应激、内质网应激、Notch因子的关系,从而揭示急性胰腺炎细胞凋亡的发生机制.Acute pancreatitis （AP） is a common critical illness in clinic. Its pathogenesis is complex. Previous studies concentrated on inflammatory factors, oxidative stress, microcirculation disturbance, etc. Recently, apoptosis has been found to play an important role in emergence and development of acute pancreatitis. Apoptosis is involved in tissue injury in acute pancreatitis, but is also an important selfJ protection mechanism. This review briefed the relation between apoptosis and acute pancreatitis, investigated the influence of apoptosis on acute pancreatitic organ damage,and analyzed the relation between apoptosis and inflammatory cytokines, oxidative stress, endoplasmic reticulum stress, Notch factor, aiming at revealing the mechanism of apoptosis in acute pancreatitis.

关 键 词：急性胰腺炎 细胞凋亡 机制 炎症因子 氧化应激 内质网应激 

分 类 号：R576[医药卫生—消化系统]