PI3K／Akt通路在脑缺血Bad线粒体转位中的神经保护作用  

Neuroprotective effects of PI3K/Akt pathway on Bad mitochondrial translocation in cerebral ischemia

作　　者：王晓天[1] 刘晓梅[1] 尤红娟[1] 李小翠[1] 秦苏萍[1] 汤仁仙[1] 郑葵阳[1] 

机构地区：[1]徐州医学院病原生物学与免疫学教研室,江苏徐州221004

出　　处：《徐州医学院学报》2014年第11期715-718,共4页Acta Academiae Medicinae Xuzhou

基　　金：国家自然科学基金（81171590）;江苏省教育厅科技基金（14KJB310023）.

摘　　要：目的探讨磷脂酰肌醇-3激酶／蛋白激酶B（phosphatidylinositol 3-kinase／Akt，P13K／Akt）通路在缺血性脑中风B细胞白血病-2（Bcell lewkmia-2，Bcl-2）细胞死亡受体拮抗剂（antagonistofcelldeath，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CAl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CAl区神经元Bad与Aktl的结合增多，Bad与B—cell lymphoma—extralarge（Bcl-X1）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P13K／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。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 immunoprecip- itation 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 - X1）, 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 ap- optosis in rats after cerebral I/R.

关 键 词：BAD PI3K AKT 凋亡 脑缺血 

分 类 号：R743.31[医药卫生—神经病学与精神病学]