丁基苯酞对大鼠脑缺血／再灌注后海马CAl区Akt磷酸化的影响  

Effects of N - butylphthalide on the phosphorylation of Akt in the hippocampal CA1 regions of rats after focal cerebral ischemia/reperfusion

作　　者：温相如[1,2] 徐洲[1] 宋远见[2] 朱广远 徐楚潇 丁佳吉 刘红芝[2] 刘永民[1] 张荣丽[1] 

机构地区：[1]徐州医学院公共教育学院,江苏徐州221004 [2]徐州医学院神经生物学研究中心 [3]徐州医学院临床学院2011级

出　　处：《徐州医学院学报》2014年第11期719-721,共3页Acta Academiae Medicinae Xuzhou

基　　金：国家自然科学基金（30800446）;江苏省教育厅面上基金（11KJB310013）;江苏省大学生创业重点课题（201310313023Z）.

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CAl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CAl区神经元细胞凋亡的影响。结果缺血／再灌注6h丁基苯酞组其Akt的磷酸化明显提高（P〈O．05），丁基苯酞对CAl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。Objective To investigate whether N - butylphthalide retards neural apoptosis via activating Akt in the hippocampal CA1 region of rats after focal cerebral isehemia/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 hippocam- pal CA1 region. Conclusion N - butylphthalide may suppress neural apoptosis in rats after ischemia/reperfusion via en- hancing the phosphorylation of Akt.

关 键 词：丁基苯酞 脑缺血/再灌注 蛋白激酶B 脑损伤 

分 类 号：R743.31[医药卫生—神经病学与精神病学]