《生命科学》 2015, 27(7): 922-927

解偶联蛋白与阿尔茨海默病

张　军1，于　霄1，郭　羽1，吴　琼2，邹　原2*

(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)

摘　要：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 and Alzheimer’s disease

ZHANG Jun1， YU Xiao1， GUO Yu1， WU Qiong2， ZOU Yuan2*

(1 Department of Pathology， Dalian Medical University， Dalian 116044， China; 2 Department of Physiology， Dalian Medical University， Dalian 116044， China)

Abstract: Abstract: 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.