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线粒体解偶联蛋白(uncoupling proteins,UCPs)是线粒体载体蛋白家族的一个亚族,位于线粒体内膜,可以将线粒体内膜外的质子转运回基质,降低线粒体的跨膜质子电动势,形成质子漏,使氧化磷酸化解偶联,ATP生成减少。目前共发现有5个成员,UCP1仅存在于棕色脂肪组织,主要参与机体非震颤产热;UCP2,UCP4和UCP5(又名脑线粒体膜载体蛋白1)在脑组织中表达较多。近年来UCPs在脑缺血缺氧性损伤中的病理生理作用研究较多,但也颇多争议。有人认为UCPs通过解偶联作用加重能量衰竭,进一步促进脑缺血缺氧损伤;也有人认为UCPs通过调节线粒体膜电位,抑制活性氧簇生成,维持线粒体内钙稳态,从而起到对神经系统的保护作用。
Mitochondrial uncoupling proteins (UCPs), a subfamily of mitochondrial carrier protein families, are located in the mitochondrial inner membrane and transport the protons outside the mitochondrial inner membrane back to the matrix, reducing the transmembrane proton electromotive force of the mitochondria to form a proton leak, Decoupling oxidative phosphorylation reduces ATP production. At present, a total of 5 members have been found, UCP1 is only present in brown adipose tissue and mainly involved in non-tremor fever. UCP2, UCP4 and UCP5 (also known as mitochondrial membrane protein carrier 1) are expressed more in brain tissue. In recent years, UCPs in the pathophysiology of cerebral ischemia and hypoxia injury more, but also quite controversial. Some people think that UCPs can aggravate energy failure through uncoupling and further promote cerebral ischemia and hypoxia injury. Some people think that UCPs can regulate the mitochondrial calcium homeostasis by regulating the mitochondrial membrane potential and thus stabilize the nervous system The protective effect.