解偶联蛋白与阿尔茨海默病  

Uncoupling protein and Alzheimer's disease

作　　者：张军[1] 于霄[1] 郭羽[1] 吴琼[2] 邹原[2] 

机构地区：[1]大连医科大学病理学教研室,大连116044 [2]大连医科大学生理学教研室,大连116044

出　　处：《生命科学》2015年第7期922-927,共6页Chinese Bulletin of Life Sciences

基　　金：辽宁省教育厅科研项目(L2012329);国家自然科学基金项目(81071725)

摘　　要：解偶联蛋白(uncoupling protein,UCP)是线粒体内膜上的质子转运蛋白,被激活时能引发质子漏,质子经UCP渗漏回基质,使氧化磷酸化部分解耦联,降低线粒体膜电位,减少过量活性氧的产生。另外,UCP对ATP合成、钙离子稳态、能量代谢等也有调节作用。阿尔茨海默病是一种中枢神经系统退行性疾病,由多种因素共同作用引起,其中活性氧的作用越来越引起重视。UCP,特别是UCP2在中枢神经系统疾病方面的保护作用日益引起关注,有望成为阿尔茨海默病治疗的靶向目标。Uncoupling protein （UCP） is the mitochondrial inner membrane carrier protein. When the concept of mild uncoupling has been introduced, UCP predicts the existence of a protein-regulated proton leak with the main purpose of controlling mitochondrial oxidative stress, and reducing the generation of superoxide anion. In addition, UCP interferes with ATP synthesis, as a potential modulator of mitochondrial Ca2＋ uptake and energy metabolism. Alzheimer＇s disease （AD） is progressively neurodegenerative disorder. A large number of studies have shown that reactive oxygen species （ROS） plays a significant role in AD pathogenesis. UCP has an important impact on mitochondrial ROS production, ATP generation and calcium regulation, suggesting that UCP, especially UCP2, may be a potential target for AD treatment.

关 键 词：解偶联蛋白2 阿尔茨海默病 活性氧 

分 类 号：Q71[生物学—分子生物学] R749.16[医药卫生—神经病学与精神病学]