摘要
活性氧(ROS)引起的氧化损伤在糖尿病并发症的发病机制中起重要作用。最新研究显示,线粒体ROS增加可能是糖尿病并发症发病的共同机制。因此,减少线粒体ROS生成及其引起的氧化损伤,为糖尿病并发症的防治提供了新策略。这一新策略有望通过设计线粒体靶向性抗氧化剂及减少线粒体膜电位的药物来实现。文章简述线粒体氧化损伤的背景,并就线粒体靶向性抗氧化剂及解耦联蛋白在糖尿病并发症的防护作用进行探讨。
Oxidative damage resulting from rective oxygen species （ROS） plays an important role in the mechanism of di- abetic complication. Recent studies showed that increased ROS in mitochondria maybe the common pathogenesy of diabetic com-plication. So, reducing the genesis of ROS in mitochondria and oxidative damage resulting from it will provide a new idea for the prevention and therapy of diabetic complication. This new strategy maybe achieved by designing mitochondria-targeted antioxi-dant and drugs reducing the mitochondrial membrane potential. This article reviews the background of mitechondrial oxidative damage, and debates the r^rotective effect of mitochondria-tarzeted antioxidant and uncouulin~ nrotein on diabetic comnlication
出处
《医学综述》
2007年第24期1973-1975,共3页
Medical Recapitulate
关键词
线粒体
活性氧
糖尿病并发症
药靶
抗氧化剂
解耦联蛋白
Mitochondria
Reactive oxygen species
Diabetic complications
Pharmacological target
Antioxidants
Un-coupling protein
