内质网应激、肠黏膜屏障与炎症性肠病  

Endoplasnic reticulum stress zntestinal mucosal barrier and inflammatory bowel disease

作　　者：郝献华[1] 龚剑峰[1] 李宁[1] 

机构地区：[1]南京大学医学院临床学院(南京军区南京总医院)解放军普通外科研究所,江苏南京210002

出　　处：《肠外与肠内营养》2011年第1期50-53,共4页Parenteral & Enteral Nutrition

基　　金：国家自然科学基金项目(30901420)

摘　　要：未折叠蛋白在内质网中大量蓄积引起的内质网应激(ERS),可能是引起炎症性肠病(IBD)的关键机制,受到人们广泛的关注。肠上皮细胞分泌功能高,极易受ERS的影响。上皮细胞未折叠蛋白反应(UPR)途径的自身缺陷或细胞内错误折叠蛋白产生过多,都可引起ERS,导致肠黏膜屏障损伤和肠黏膜炎症。而肠腔共生菌群和黏膜炎性因子等,都可通过调节上皮ERS影响IBD的发生。而上皮ERS可与自噬过程协同作用,影响ERS的最终结局。The endoplasmic reticulum（ER） responds to the accumulation of unfolded proteins in its lumen（ER stress） by activating intracellular signal transduction pathways-cumulatively called the unfolded protein response（UPR）,which has recently been implicated as a novel mechanism that may lead to inflammatory bowel disease（IBD）.Impairment of proper ER stress resolution in intestinal epithelium can primarily lead to inflammation.Failing to manage ER stress may not only be a primary originator of intestinal inflammation as exemplified by genetic polymorphisms in XBP1 that are associated with IBD but also a perpetuator of inflammation when ER stress is induced secondarily to inflammation mediators or microbial factors.Furthermore,ER stress pathways may interact with other processes that lead to IBD,notably autophagy.

关 键 词：炎症性肠病 内质网应激 未折叠蛋白反应 

分 类 号：R574[医药卫生—消化系统]