【摘要】 目的 探讨磷脂酰肌醇-3激酶/蛋白激酶B(phosphatidylinositol 3-kinase/Akt,PI3K/Akt)通路在缺血性脑中风B细胞白血病-2(B cell lewkmia-2,Bcl-2)细胞死亡受体拮抗剂(antagonist of cell death,Bad)线粒体转位及神经元凋亡中的重要作用。方法 制作大鼠全脑缺血模型,腹腔注射bpV(pic),应用免疫沉淀和免疫印迹法检测脑缺血复灌1天海马CA1区神经元Bad线粒体转位和细胞色素c释放,TUNEL法检测复灌3天神经元凋亡。结果 与缺血复灌组和溶剂对照组相比,bpV(pic)组海马CA1区神经元Bad与Aktl的结合增多,Bad与B-cell lymphoma-extra large(Bcl-Ⅺ)的结合、线粒体细胞色素c的释放和神经元凋亡明显减少(P <0.05)。结论 PI3 K/Akt通路在大鼠脑缺血复灌Bad线粒体转位及神经元凋亡中发挥了重要作用。更多还原

【Abstract】 Objective To investigate the effects of the phosphatidylinositol 3-kinase/Akt(PI3K/Akt) pathway on Bcl-2 antagonist of cell death(Bad) mitochondrial translocation and neuronal apoptosis in ischemic stroke.Methods A rat model of cerebral ischemia was established where bpV(pic) were intraperitoneally injected.Then the Bad mitochondrial translocation and the release of cytochrome c in the hippocampal CA1 region were detected using immunoprecipitation and immunoblotting one day after ischemia/reperfusion(I/R).Neuronal apoptosis was detected by TUNEL assay three days after I/R.Results Compared with the I/R and solvent control groups,enhanced binding of Bad and Aktl was observed within the hippocampal CA1 region of the bpV(pic) group.Meanwhile,the binding of Bad and B-cell lymphoma-extra large(Bcl-Xl),the release of cytochrome c and neuronal apoptosis were obviously decreased(P <0.05).Conclusion The PI3K/Akt pathway takes an important role in Bad mitochondrial translocation and neuronal apoptosis in rats after cerebral I/R.更多还原