内质网应激信号分子PERK在溃疡性结肠炎肠黏膜损伤中的研究进展  

Role of endoplasmic reticulum stress signaling molecule PERK in bowel mucosal injury in ulcerative colitis

作　　者：郑烈[1] 戴彦成[1] 张亚利[2] 陈璇[1] 方晨晔 唐志鹏[1,2] 

机构地区：[1]上海中医药大学附属龙华医院消化内科,上海市200032 [2]上海中医药大学脾胃病研究所,上海市200032

出　　处：《世界华人消化杂志》2015年第34期5493-5498,共6页World Chinese Journal of Digestology

基　　金：国家自然科学基金资助项目;Nos.81573892;81403355~~

摘　　要：内质网应激(endoplasmic reticulum stress,ERS)是研究溃疡性结肠炎(ulcerative colitis,UC)发病机制的主要热点,通过启动未折叠蛋白反应(unfolded protein response,UPR)来保护和修复肠道黏膜上皮细胞的损伤.内质网应激主要通过三种信号通路来介导炎性因子的分泌,其中蛋白激酶R样内质网激酶(protein kinase R-like ER kinase,PERK)通路与UC发病关系最为密切.肠道黏膜上皮细胞(intestinal mucosa epithelial cells,IEC)具有发达的内质网结构,是代谢最为旺盛的细胞群之一.持续严重的ERS促使细胞损伤、死亡,导致肠黏膜上皮细胞激活核因子-kB(nuclear factor-kB,NF-kB),引起多种炎性因子的分泌,促进炎症病变的发生.中药治疗UC疗效显著,有其独特优势,可通过信号通路抑制NF-kB炎性因子分泌,保护肠道屏障功能.Endoplasmic reticulum stress（ERS） is the main focus in the study of the pathogenesis of ulcerative colitis,and it protects and repairs the intestinal epithelial cell（IEC） injury through unfolded protein response（UPR）.Protein kinase R-like ER kinase（PERK） is an endoplasmic reticulum-localized type I transmembrane protein,with serine/threonine protein kinase activity.IECs are one of cell populations with the most vigorous metabolism and have abundant endoplasmic reticulum.Early ERS can activate PERK-elF2 alpha channel and inhibit the synthesis of proteins to protect cells.However,sustained severe ERS promotes cell damage and death,activates nuclear factor-kappa B in IECs,causes the secretion of a variety of inflammatory cytokines,and promotes the occurrence of inflammatory lesions.

关 键 词：内质网应激 溃疡性结肠炎 PERK-eIF2a信号通路 肠道黏膜上皮细胞 核因子-KB 

分 类 号：R574.62[医药卫生—消化系统]