中文摘要：

目的观察小鼠脑缺血再灌注后缝隙连接蛋白43（Cx43）表达变化及缝隙蛋白阻断剂辛醇对小鼠梗死体积的影响。方法采用线栓法制备小鼠大脑中动脉阻塞模型（MCAO模型），应用免疫印迹（Westernblot）方法观察脑缺血再灌注损伤前后Cx43表达变化和辛醇对Cx43表达的影响，并计算各组死亡率及脑梗死体积。结果小鼠脑缺血2h再灌注损伤24h条件下，缺血区Cx43表达在损伤前后无明显变化（P〉0．05）。辛醇能显著抑制脑缺血再灌注损伤后Cx43表达，降低死亡率及减少脑梗死体积，具有统计学差异（P〈0．05）。结论由Cx43组成的缝隙连接蛋白在脑缺血再灌注损伤过程中具有重要作用，缝隙蛋白-43阻断剂辛醇通过抑制海马及皮质Cx43表达，进而降低死亡率及梗死体积，从而发挥神经保护作用。

英文摘要：

Objective To observe the expression change of Cx43 after ischemia-reperfusion in mouse brain and the influence of slit protein blocking agent octanol on mouse infarct volume. Methods Mouse model of middle cerebral artery occlusion （MCAO model）was prepared by thread embolism method. Using the Western blot method （Western blot） , expression changes of Cx43 after cerebral isehemia-reperfusion injury and the effect of alcohoi on Cx43 expression was observed, and their mortality and cerebral infarction volume were calculated. Results In 24h of mouse cerebral ischemia reperfusion injury, Cx43 expression in the isehemic area damage showed no significant difference before and after injury （ P 〉 0.05 ）. Octanol could significantly inhibit Cx43 expression after the cerebral ischemia reperfusion injury, reduced the mortality and the volume of cerebral infarction, and had significant difference （ P 〈 0.05 ）. Conclusion Gap junctional proteins consisting of Cx43 plays an important role in cerebral ischemia reperfusion injury. Slit protein-43 blocker octanol inhibits the expression of Cx43 in hippocampus and cortex, and to reduce mortality and infarction volume, thus plays a neuroprotective role.