【摘要】 目的 探讨丁基苯酞是否通过对大鼠脑缺血/再灌注后海马CA1区蛋白激酶B(Akt)磷酸化的影响而延缓了海马神经元的死亡。方法 四动脉结扎法建立大鼠脑缺血模型,采用免疫印迹法检测丁基苯酞对脑缺血/再灌注注后信号蛋白Akt磷酸化的影响;采用末端脱氧核苷酸转移酶(TdT)介导的d-UTP缺口末端标记(TUNEL)技术观察脑缺血/再灌注注后丁基苯酞对海马CA1区神经元细胞凋亡的影响。结果 缺血/再灌注6 h丁基苯酞组其Akt的磷酸化明显提高(P<0.05),丁基苯酞对CA1区神经元具有保护作用(P<0.05)。结论 丁基苯酞增强脑缺血/再灌注后Akt的磷酸化可能是其对大鼠缺血/再灌注性脑损伤保护作用的机制之一。更多还原

【Abstract】 Objective To investigate whether N-butylphthalide retards neural apoptosis via activating Akt in the hippocampal CA1 region of rats after focal cerebral ischemia/reperfusion.Methods A rat model of cerebral ischemia was induced by occlusion of bilateral common carotid and vertebral arteries.After cerebral ischemia/reperfusion,the effects of N-butylphthalide on the phosphorylation of Akt in the hippocampal CA1 regions of rats were examined using Western blotting.After administration of N-butylphthalide,the neural apoptosis in the hippocampal CA1 region was detected by TUNEL method.Results After six hours of reperfusion,the phosphorylation of Akt were remarkably enhanced in the N-butylphthalide group(P <0.05).N-butylphthalide could obviously reduce neural apoptosis in the hippocampal CA1 region.Conclusion N-butylphthalide may suppress neural apoptosis in rats after ischemia/reperfusion via enhancing the phosphorylation of Akt.更多还原