溃疡性结肠炎发病新机制以及热休克蛋白65的作用  

The New Pathogenesis of Ulcerative Colitis and the Effect of Heat Shock Protein 65 on Ulcerative Colitis

作　　者：董颖[1] 邵圣文[1] 王莎[1] 杨红霞 

机构地区：[1]湖州师范学院医学院,浙江湖州313000 [2]湖州市食品药品检验研究院,浙江湖州313000

出　　处：《湖州师范学院学报》2017年第8期79-83,共5页Journal of Huzhou University

基　　金：浙江省公益性技术应用研究实验动物计划项目(2016C37126)

摘　　要：溃疡性结肠炎是一种肠道非特异慢性炎症疾病,被世界卫生组织列为难治疾病,目前尚无特效治疗手段.溃疡性结肠炎病因和发病机制尚不十分清楚,限制了治疗药物的开发.对肠道菌群、热休克蛋白家族在溃疡性结肠炎发病中的作用以及热休克蛋白65的潜在治疗作用,以期加深对溃疡性结肠炎发病机制认识,为寻找潜在治疗靶点及药物开发提供借鉴.Ulcerative colitis（UC）is a non-specific chronic inflammation of gut,listed as a kind of refractory disease by the world health organization,and up to now there is no special treatment for UC.Because the pathogenesis of UC has not been known clearly,the development of drug for UC is also restrainted.This review studies the effect of gut microbiota and heat shock protein families on the pathogenesis of UC,and the potential therapeutic effects of heat shock protein 65 for UC have also been studied.This review enhances the understanding to UC pathogenesis and provides clues to potential therapeutic targets and development of drug for UC treatment.

关 键 词：溃疡性结肠炎 热休克蛋白65 肠道菌群 免疫异常 

分 类 号：R574[医药卫生—消化系统]