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首页> 美国卫生研究院文献>Journal of Cerebral Blood Flow Metabolism >Protective effect of delayed remote limb ischemic postconditioning: role of mitochondrial KATP channels in a rat model of focal cerebral ischemic reperfusion injury
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Protective effect of delayed remote limb ischemic postconditioning: role of mitochondrial KATP channels in a rat model of focal cerebral ischemic reperfusion injury

机译：迟发性远端肢体缺血后处理的保护作用：线粒体KATP通道在局灶性脑缺血再灌注损伤大鼠模型中的作用

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摘要

Delayed remote ischemic postconditioning (DRIPost) has been shown to protect the rat brain from ischemic injury. However, extremely short therapeutic time windows hinder its translational use and the mechanism of action remains elusive. Because opening of the mitochondria KATP channel is crucial for cell apoptosis, we hypothesized that the neuroprotective effect of DRIPost may be associated with KATP channels. In the present study, the neuroprotective effects of DRIPost were investigated using adult male Sprague-Dawley rats. Rats were exposed to 90 minutes of middle cerebral artery occlusion followed by 72 hours of reperfusion. Delayed remote ischemic postconditioning was performed with three cycles of bilateral femoral artery occlusion/reperfusion for 5 minutes at 3 or 6 hours after reperfusion. Neurologic deficit scores and infarct volumes were assessed, and cellular apoptosis was monitored by terminal deoxynucleotidyl transferase nick-end labeling. Our results showed that DRIPost applied at 6 hours after reperfusion exerted neuroprotective effects. The KATP opener, diazoxide, protected rat brains from ischemic injury, while the KATP blocker, 5-hydroxydecanote, reversed the neuroprotective effects of DRIPost. These findings indicate that DRIPost reduces focal cerebral ischemic injury and that the neuroprotective effects of DRIPost may be achieved through opening of KATP channels.
机译：延迟远程缺血后处理（DRIPost）已被证明可以保护大鼠脑免受缺血性损伤。然而，极短的治疗时间窗阻碍了其翻译使用，并且作用机理仍然难以捉摸。因为线粒体KATP通道的开放对于细胞凋亡至关重要，所以我们假设DRIPost的神经保护作用可能与KATP通道有关。在本研究中，使用成年雄性Sprague-Dawley大鼠研究了DRIPost的神经保护作用。将大鼠暴露于大脑中动脉闭塞90分钟，然后再灌注72小时。在再灌注后的3或6小时内，通过三个周期的双侧股动脉闭塞/再灌注进行5分钟，进行延迟的远程缺血后处理。评估神经功能缺损评分和梗塞体积，并通过末端脱氧核苷酸转移酶缺口末端标记监测细胞凋亡。我们的研究结果表明，DRIPost在再灌注后6小时施用具有神经保护作用。 KATP开环剂二氮嗪可保护大鼠大脑免受缺血性损伤，而KATP阻断剂5-羟基癸香可逆转DRIPost的神经保护作用。这些发现表明DRIPost减少了局灶性脑缺血损伤，并且DRIPost的神经保护作用可以通过打开KATP通道来实现。

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