线粒体ATP敏感性钾通道在糖尿病合并脑缺血损伤中作用的研究进展  

The research progress of mito KATPin diabetes with cerebral ischemic injury

作　　者：施宁华[1] 韩江全[1] 邓才洪 何婧[1] SHI Ning-hua;HAN Jiang-quan;DENG Cai-hong;HE jing(Department of Neurology,the Fifth Affiliated(Zhuhai)Hospital,Zunyi Medical College,Zhuhai 519100,China)

机构地区：[1]广东省珠海市遵义医学院第五附属(珠海)医院神经内科,519100

出　　处：《天津医药》2018年第7期776-780,共5页Tianjin Medical Journal

摘　　要：糖尿病是脑血管疾病重要的独立危险因素,大量的临床和实验研究证实,糖尿病可加重脑缺血损伤,但其机制尚不十分清楚。线粒体ATP敏感性钾通道(mitoK_(ATP))是位于线粒体内膜上一种重要的离子通道,在许多生理病理过程中发挥重要功能。近年来,不断有研究表明,mitoK_(ATP)对脑缺血损伤有保护作用,而糖尿病可使其启动的正常保护机制受损,mitoK_(ATP)与糖尿病合并脑缺血损伤的关系受到大家越来越多的关注。本文就mitoK_(ATP)在糖尿病合并脑缺血损伤中的作用作一综述。Diabetes is an important independent risk factor for cerebrovascular diseases.A large number of clinical and experimental studies have confirmed that diabetes can aggravate cerebral ischemic injury,but the mechanism is not yet clear.Mitochondrial ATP-sensitive potassium channel(mitoKATP)is an important ion channel located in the mitochondrial inner membrane,playing very important roles in many physiological and pathological processes.In recent years,studies have showed that mitoKATP has a protective effect on cerebral ischemic neuronal injury,but its protective mechanism is abolished in diabetes.The relationship between mitoKATP and diabetes with cerebral ischemic injury has attracted more and more attention.In this article,the role of brain mitoKATP in diabetes with cerebral ischemic injury was reviewed.

关 键 词：糖尿病 脑缺血 KATP通道 线粒体 综述 

分 类 号：R743[医药卫生—神经病学与精神病学]