Liang Jian-min, Xu Hai-yang, Zhang Xiao-jie, Li Xungeng, Zhang Hong-bo, Ge Peng-fei
Department of Peediatrics, First Bethune Hospital of Jilin University, Changchun, China.
J Int Med Res. 2013 Jun;41(3):618-27. doi: 10.1177/0300060513476587. Epub 2013 Apr 4.
To investigate the effects of ischaemic postconditioning on brain injury and mitochondria in focal ischaemia and reperfusion, in rats.
Adult male Wistar rats (n = 15 per group) underwent sham surgery, ischaemia (2-h middle cerebral artery occlusion), or ischaemia followed by ischaemic postconditioning (three cycles of 30 s reperfusion/30 s reocclusion). Brain infarction size, neurological function, mitochondrial reactive oxygen species (ROS) production, mitochondrial membrane potential and mitochondrial swelling were evaluated 24 h postsurgery.
Infarct size was significantly smaller, and neurological function was significantly better, in the ischaemic postconditioning group than in the ischaemia group. Ischaemia resulted in significant increases in mitochondrial ROS production and swelling, and a reduction in mitochondrial membrane potential, all of which were significantly reversed by postconditioning.
The protective role of ischaemic postconditioning in focal ischaemia/reperfusion may be due to decreased mitochondrial ROS production, reduced mitochondrial membrane potential and suppressed mitochondria swelling. Mitochondria are potential targets for new therapies to prevent brain damage caused by ischaemia and reperfusion.
研究缺血后处理对大鼠局灶性缺血再灌注脑损伤及线粒体的影响。
成年雄性Wistar大鼠（每组15只）接受假手术、缺血（大脑中动脉闭塞2小时）或缺血后进行缺血后处理（30秒再灌注/30秒再闭塞共三个周期）。术后24小时评估脑梗死体积、神经功能、线粒体活性氧（ROS）生成、线粒体膜电位及线粒体肿胀情况。
缺血后处理组的梗死体积明显较小，神经功能明显更好。缺血导致线粒体ROS生成和肿胀显著增加，线粒体膜电位降低，而后处理可使所有这些情况显著逆转。
缺血后处理对局灶性缺血/再灌注的保护作用可能是由于线粒体ROS生成减少、线粒体膜电位降低及线粒体肿胀受到抑制。线粒体是预防缺血再灌注所致脑损伤新疗法的潜在靶点。
