PI3K/Akt信号通路在肢体缺血后处理减轻脑缺血再灌注损伤中的实验研究  

The effects of PI3K/Akt signal transduction path way in the limb ischemic postconditioning against cerebral ischemia reperfusion injury

作　　者：王国峰 刘伯芹 王滨[2] 官明德 WANG Guofeng;LIU Boqin;WANG Bin(Department of Neurology,Qingdao Municipal Hospital,Qingdao 266002,China)

机构地区：[1]青岛市市立医院西院区神经内科,山东青岛266002 [2]青岛市市立医院急诊科,山东青岛266002

出　　处：《中风与神经疾病杂志》2018年第11期983-988,共6页Journal of Apoplexy and Nervous Diseases

摘　　要：目的通过观察远程肢体缺血后处理后p-Akt、Caspase-9及Bcl-2的表达,探讨PI3K/Akt信号通路在肢体缺血后处理减轻脑缺血再灌注损伤中的作用。方法 42只Wistar大鼠随机分成对照组、缺血再灌注(IR)组和肢体缺血后处理(LIP)组,后两组采用线栓法制备局灶性脑缺血再灌注模型,LIP组在缺血2 h后再灌注前实施3个循环健侧股动脉5 min缺血5 min再灌注的肢体缺血后处理。采用TTC染色测定脑梗死体积,免疫组织化学法检测p-Akt、Caspase-9、Bcl-2蛋白表达、原位杂交法检测Caspase-9、Bcl-2 mRNA的表达。结果 LIP组大鼠梗死体积较IR组明显减小(P <0. 05)。LIP组p-Akt、Bcl-2表达较IR组明显增高(P <0. 05),LIP组Caspase-9表达较IR组明显降低(P <0. 05)。结论远程肢体缺血后处理可上调p-Akt、Bcl-2表达,下调Caspase-9表达,减轻脑梗死体积,PI3K/Akt信号通路可能在肢体缺血后处理减轻脑缺血再灌注损伤中发挥了重要作用。Objective To investigate the expression changes of the p-Akt,caspase-9,Bcl-2 in the rats model of limb ischemic postconditioning( LIP),and examine the effect of the phosphatidylinositol 3-kinase/Protein Kinase B( PI3K/Akt)signal transduction path way in LIP against cerebral ischemia reperfusion injury in the rats. Methods 42 Wistar rats were randomly assigned to three groups: sham surgery,ischemia/reperfusion( IR) and LIP group. Two hours after the middle cerebral artery occlusion model was established in rats and then LIP was carried out by three cycles of 5 minutes occlusion/5 minutes release of the left femoral artery at the beginning of the reperfusion. Brain sections were stained with TTC for surveying the volume of infraction. The expressions of p-Akt,caspase-9,Bcl-2 protein were determined by immunohistochemical staining. The expressions of caspase-9,Bcl-2 mRNA were determined by in situ hybridization. Results Compared with the IR group,the infarct volume significantly decreased in LIP group( P < 0. 05). The expressions of p-Akt and Bcl-2 significantly increased in LIP group compared with IR group( P < 0. 05). The expression of caspase-9 significantly decreased in LIP group( P < 0. 05). Conclusion Limb ischemic postconditioning upregulated the expressions of p-Akt and Bcl-2,decreased the expressions of caspase-9,and reduced the cerebral infarct volume. PI3K/Akt signal transduction path way may play important roles in limb ischemic postconditioning against cerebral ischemia reperfusion injury.

关 键 词：肢体缺血后处理 磷脂酰肌醇3激酶 丝-苏氨酸蛋白激酶 缺血再灌注 

分 类 号：R743[医药卫生—神经病学与精神病学]