School of Biomedical Sciences, The University of Queensland, Brisbane, QLD 4072, Australia.
Neurochem Int. 2013 Apr;62(5):712-8. doi: 10.1016/j.neuint.2012.11.009. Epub 2012 Nov 29.
Oxidative stress has emerged as a key deleterious factor in brain ischemia and reperfusion. Malfunction of the oxidative respiratory chain in mitochondria combines with the activation of cytoplasmic oxidases to generate a burst of reactive oxygen species that cannot be neutralised by the cell's antioxidant mechanisms. As a result, oxidative stress contributes directly to necrosis and apoptosis through a number of pathways in ischemic tissue. Pharmacological intervention with antioxidants or enhancers of endogenous antioxidant molecules is proving to be difficult due to the speed and scope of the oxidative impact. Additionally, the knowledge that neuronal fate in ischemic stroke is tightly linked to other brain cells like endothelial cells and astrocytes has shifted the focus of study from isolated neurons to the neurovascular unit. For this reason, recent efforts have been directed towards understanding the sources of oxidative stress in ischemic stroke and attempting to block the generation of oxygen radicals.
氧化应激已成为脑缺血再灌注的一个关键有害因素。线粒体氧化呼吸链的功能障碍与细胞质氧化酶的激活相结合，产生大量无法被细胞抗氧化机制中和的活性氧。因此，氧化应激通过缺血组织中的多种途径直接导致坏死和细胞凋亡。由于氧化作用的速度和范围，用抗氧化剂或内源性抗氧化分子的增强剂进行药物干预被证明是困难的。此外，人们认识到，缺血性中风中神经元的命运与内皮细胞和星形胶质细胞等其他脑细胞紧密相连，这使得研究的重点从孤立的神经元转移到了神经血管单元。出于这个原因，最近的努力方向是了解缺血性中风中氧化应激的来源，并试图阻止氧自由基的产生。
