Xing Bianzhi, Chen Hui, Zhang Min, Zhao Dongming, Jiang Rui, Liu Xiuheng, Zhang Suming
Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Hang Kong Road 13, Wuhan, 430030, China.
Stroke. 2008 Aug;39(8):2362-9. doi: 10.1161/STROKEAHA.107.507939. Epub 2008 Jun 26.
Ischemic postconditioning (Postcond) is defined as a series of intermittent interruptions of blood flow in the early phase of reperfusion that mechanically alters the hydrodynamics of reperfusion. A recent study showed that Postcond reduced infarct size in cerebral ischemia/reperfusion (I/R) injury. However, little is known about the mechanisms of Postcond in cerebral I/R injury. In the present study, we investigated the effects of Postcond in focal cerebral I/R injury in the rat middle cerebral artery occlusion model.
Adult male Sprague-Dawley rats were treated with Postcond after 60 minutes of occlusion (beginning of reperfusion). Neurologic scores and infarct volumes were assessed at 24 and 72 hours. Oxidative stress was evaluated by malondialdehyde assay, and apoptosis-related molecules were studied by Western blotting.
Postcond treatment upregulated Bcl-2 and heat-shock protein 70 expression and downregulated cytochrome c release to the cytosol, Bax translocation to the mitochondria, and caspase-3 activity. Postcond treatment also reduced infarct volumes and oxidative stress levels and improved neurologic scores compared with the I/R-only group.
These findings indicate that Postcond inhibits focal cerebral I/R injury. This neuroprotective effect is likely achieved by antiapoptotic mechanisms.
缺血后处理（Postcond）被定义为在再灌注早期进行的一系列间歇性血流中断，其通过机械方式改变再灌注的流体动力学。最近一项研究表明，缺血后处理可减小脑缺血/再灌注（I/R）损伤中的梗死灶大小。然而，关于缺血后处理在脑I/R损伤中的机制却知之甚少。在本研究中，我们在大鼠大脑中动脉闭塞模型中研究了缺血后处理对局灶性脑I/R损伤的影响。
成年雄性Sprague-Dawley大鼠在闭塞60分钟后（再灌注开始时）接受缺血后处理。在24小时和72小时时评估神经功能评分和梗死体积。通过丙二醛测定评估氧化应激，并通过蛋白质印迹法研究凋亡相关分子。
缺血后处理上调了Bcl-2和热休克蛋白70的表达，并下调了细胞色素c向细胞质的释放、Bax向线粒体的转位以及caspase-3活性。与单纯I/R组相比，缺血后处理还减小了梗死体积，降低了氧化应激水平，并改善了神经功能评分。
这些发现表明，缺血后处理可抑制局灶性脑I/R损伤。这种神经保护作用可能是通过抗凋亡机制实现的。
