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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(Western blot)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。
Objective To observe the changes of connexin-43 (Cx43) expression and infarct volume of mice after cerebral ischemia-reperfusion. Methods The middle cerebral artery occlusion model (MCAO) was established by thread occlusion. The expression of Cx43 and the expression of Cx43 in cerebral ischemia-reperfusion injury were observed by Western blot. Mortality and infarct volume. Results The expression of Cx43 in the ischemic area had no significant change before and after ischemia (P> 0.05). Octanol can significantly inhibit the expression of Cx43 after cerebral ischemia-reperfusion injury, reduce mortality and reduce the volume of cerebral infarction, with statistical significance (P <0.05). Conclusion The connexin with Cx43 plays an important role in the process of cerebral ischemia-reperfusion injury. The expression of Cx43, a gap-4 inhibitor, inhibits the expression of Cx43 in the hippocampus and cortex, thereby reducing the mortality and the infarct volume, thus playing a neuroprotective role effect.