氨甲酰化促红细胞生成素经PI3-K/Akt信号通路抗脑缺血损伤  被引量:7

Carbamylated erythropoietin via PI3-K/Akt signaling pathway reduces cerebral ischemic injury

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作  者:张蓓[1] 王林[1] 柏玉兰 石少亭[1] 张雷[1] 李亚军[1] 

机构地区:[1]西安医学院第一附属医院神经内科,陕西西安710077

出  处:《中风与神经疾病杂志》2017年第6期488-490,共3页Journal of Apoplexy and Nervous Diseases

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.14JK1629);陕西省卫生厅科研基金资助项目(No.2010H27);陕西省优势学科建设项目资助

摘  要:目的观察脑缺血后氨甲酰化促红细胞生成素(CEPO)的神经保护作用并探讨其可能机制。方法健康雄性SD大鼠随机分为6组(n=10):(1)假手术组;(2)缺血组;(3)EPO组;(4)CEPO组;(5)LY(LY294002)组;(6)CEPO+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PI3-K/Akt活性变化。结果 EPO组与CEPO组脑梗死体积均明显缩小,神经功能显著改善,磷酸化Akt(p Akt)水平明显增高,且两组之间无明显差异,但CEPO的神经保护作用及对Akt磷酸化的诱导效应均可被PI3-K抑制剂LY294002部分抵消。结论 CEPO具有与EPO相当的缺血后脑保护作用,其机制可能与PI3-K/Akt信号通路激活有关。Objective To study the neuroprotective effect of carbamylated erythropoietin( CEPO) on cerebral ischemic injury and its possible mechanism. Methods Sixty healthy male SD rats were randomly divided into 6 groups( n = 10each) : sham operation group,ischemia group,EPO group,CEPO group,LY group and CEPO + LY group. Focal cerebral ischemia model of middle cerebral artery occlusion( MCAO) was established in rats using the suture method. Neurological function and the volume of cerebral infarction were evaluated on the expected time points. The changes in activity of PI3-K/Akt pathway were determined by Western blot. Results In both EPO group and CEPO group,the protein levels of phosphorylated Akt( p Akt) were increased markedly with less volume of cerebral infarction and better neurological function,and there was no significant difference between the two groups. However,the neuroprotection of CEPO and its induction of Akt phosphorylation were partially abolished by LY294002,which was the inhibitor of PI3-K. Conclusion The neuroprotective effect of CEPO is equivalent to EPO after cerebral ischemia,which may be related to the activation of PI3-K/Akt signaling pathway.

关 键 词:磷脂酰肌醇-3激酶/丝氨酸-苏氨酸蛋白激酶 促红细胞生成素 氨甲酰化促红细胞生成素 脑缺血 

分 类 号:R743.3[医药卫生—神经病学与精神病学]

 

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