脑缺血后脑红蛋白的保护作用及信号转导机制  

Neuroprotective Effect of Neuroglobin after Cerebral Ischemia and Signal Transduction Mechanism

作　　者：张蓓[1] 李亚军[1] 张世俊[1] 任会云 王敏娟[1] 郭长江[1] 

机构地区：[1]西安医学院附属医院神经内科,西安710077

出　　处：《华中科技大学学报（医学版）》2012年第5期566-568,572,共4页Acta Medicinae Universitatis Scientiae et Technologiae Huazhong

基　　金：陕西省自然科学基金资助项目(No.2010JM4054);陕西省教育厅科研基金资助项目(No.09JK713)

摘　　要：目的观察脑红蛋白(Ngb)的神经保护作用并探讨其与磷脂酰肌醇-3激酶/丝氨酸-苏氨酸蛋白激酶(PI3-K/Akt)信号通路的关系。方法健康雄性SD大鼠随机分为5组(n=12):①假手术组,②缺血组,③Hemin组,④LY(LY294002)组,⑤Hemin+LY组,应用大脑中动脉线栓法(MCAO)制作大鼠局灶性脑缺血模型,评定大鼠神经功能并计算脑梗死体积,Western blot方法检测Ngb蛋白表达和PI3-K/Akt活性变化。结果脑缺血后Ngb蛋白表达增加,Hemin可诱导Ngb高表达,磷酸化Akt(pAkt)水平亦同时升高,脑梗死体积减小,神经功能改善;LY294002特异性阻断了PI3-K/Akt信号通路的活化,加重了脑损伤,不能抑制Ngb表达。结论细胞存活信号通路PI3-K/Akt可能介导了脑缺血后Ngb的神经保护作用。Objective To study the neuroprotective effect of neuroglobin（Ngb）and the correlation between neuroglobin and PI3-K/Akt signaling pathway. Methods Sixty healthy male SD rats were randomly divided into 5 groups（n= 12 each）：sham operation group, ischemia group, Heroin group, LY group and Heroin＋ LY group. Focal cerebral ischemia model of middle cere bral artery occlusion（MCAO）was established in rats using the suture method. Neurological function and the size of cerebral in farction were evaluated on the expected time points. The expression of Ngb and the changes in activity of PI3-K/Akt pathway were determined by using Western blot. Results The protein expression levels of Ngb were increased markedly after cerebral ischemia. Heroin could induce higher expression of Ngb, meanwhile, the protein levels of phosphorylated Akt （pAkt）were in creased with less size of cerebral infarction and better neurological function. LY294002 specially blocked the activation of PI3-K/ Akt signaling pathway and aggravated brain injury,but the protein expression levels of Ngb were not inhibited. Conclusion PI3-K/Akt signaling pathway which is relevant to cell survival may mediate the neuroproteetive effect of Ngb after cerebral is chemia.

关 键 词：磷脂酰肌醇-3激酶 丝氨酸-苏氨酸蛋白激酶 脑红蛋白 脑缺血 

分 类 号：R743.3[医药卫生—神经病学与精神病学]