Ahmed Ejaz, Donovan Tucker, Yujiao Lu, Zhang Quanguang
Department of Neuroscience and Regenerative Medicine, Georgia Regents University, Augusta, GA 30912, USA.
J Neurol Neurosci. 2015;6(2). doi: 10.21767/2171-6625.100017.
There has been much evidence suggesting that reactive oxygen species (ROS) generated in mitochondria during cerebral ischemia play a major role in programming the senescence of organism. Antioxidants dealing with mitochondria slow down the appearance and progression of symptoms in cerebral ischemia and increase the life span of organisms. The mechanisms of mitochondrial targeted antioxidants, such as SKQ1, Coenzyme Q10, MitoQ, and Methylene blue, include increasing adenosine triphosphate (ATP) production, decreasing production of ROS and increasing antioxidant defenses, providing benefits in neuroprotection following cerebral ischemia. A number of studies have shown the neuroprotective role of these mitochondrial targeted antioxidants in cerebral ischemia. Here in this short review we have compiled the literature supporting consequences of mitochondrial dysfunction, and the protective role of mitochondrial targeted antioxidants.
有许多证据表明，脑缺血期间线粒体产生的活性氧（ROS）在生物体衰老编程中起主要作用。作用于线粒体的抗氧化剂可减缓脑缺血症状的出现和进展，并延长生物体的寿命。线粒体靶向抗氧化剂，如SKQ1、辅酶Q10、MitoQ和亚甲蓝的作用机制包括增加三磷酸腺苷（ATP）生成、减少ROS生成以及增强抗氧化防御，在脑缺血后的神经保护中发挥作用。多项研究已表明这些线粒体靶向抗氧化剂在脑缺血中的神经保护作用。在这篇简短的综述中，我们汇集了支持线粒体功能障碍后果以及线粒体靶向抗氧化剂保护作用的文献。
