中文摘要：

目的观察小鼠局灶性脑缺血后脑皮质神经细胞内原蛋白转化酶1（PC1）及其作用底物神经肽Y（NPY）的表达变化，探讨PCI在神经细胞缺血损伤中的作用。方法将24只雄性C57小鼠用计算机随机法分为假手术组和缺血一再灌注4、24h组，每组各8只。采用线栓法制备小鼠大脑中动脉阻塞模型，阻塞1h再灌注。采用Western Blot法、实时荧光定量核酸扩增检测小鼠脑皮质神经细胞中PCI及NPY蛋白、mRNA的表达变化。结果（1）与假手术组比较，缺血侧皮质脑组织PCImRNA缺血一再灌注4h组表达增加（2．66±0．24），缺血一再灌注24h组增加（2．07-4±0．23），差异均有统计学意义（均P〈0．05）。与假手术组比较，缺血一再灌注4h组PCI前体蛋白水平明显增加（P〈0．05），24h组差异无统计学意义（尸〉0．05）。（2）与假手术组比较，缺血一再灌注4h组前体NPY前体蛋白水平及mRNA增加（P〈0．05），mRNA表达为2．31±0．27；24h组蛋白前体水平增加（P〈0．05），NPY mRNA表达差异无统计学意义（P〉0．05）。结论小鼠脑缺血一再灌注后PCI前体表达增多，从而影响PCI的加工活性，导致PCI的作用底物NPY蛋白以前体形式堆积，可能为神经细胞缺血损伤的内在机制之一。

英文摘要：

Objectives To study the expression changes of proprotein convertase 1 （PC1） in cerebral cortex nerve cells and its substrate neuropeptide Y （NPY） after focal cerebral ischemia in mice and to investigate the effect of PC1 in neuronal ischemic injury. Methods Twenty-four male C57 mice were randomly allocated into a sham-operation group, an ischemia-reperfusion 4-or 24-hour group with computer （n = 8 in each group）. A rat model of middle cerebral artery occlusion was induced by the intraluminal suture method. Western blot and real-time quantitative nucleic acid amplification were used to detect the expression changes of PC1, NPY, and mRNA in mouse cortical neurons. Results （ ! ） Compared with the sham operation group,the expression of PC1 mRNA of ischemic cortex brain tissue at ischemic side in the ischemia-reperfusion 4-hour group increased 2.66 ±0.24 and in the ischemia-reperfusion 24-hour group expressed 2.07 ± 0.23 （ all P 〈 0.05 ）. Compared with the sham operation group, the PC1 precursor protein level increased significantly at 4 hours （ P 〈 0.05 ）. There was no significant difference in the 24-hour group （P 〉 O. 05 ）. （2）Compared with the sham operation group, the preproNPY mRNA and protein level increased significantly after reperfusion in the ischemia-reperfusion 4-hour group （ P 〈 0. 05 ） , the mRNA expressed 2.31 ± 0.27, and the increase of precursor protein level continued until 24 hours. Conclusion The expression of precursor PC1 increased after cerebral ischemia-repeffusion in mice, thus affecting the processing activity of PC1, and resulting in NPY protein, an active substrate of PC1 accumulated with the form of precursors, which may be one of the underlying mechanisms of neuronal ischemic injury.