首页 | 本学科首页   官方微博 | 高级检索  
     

PI3-K/Akt通路在脑缺血治疗中的调控机制研究
引用本文:苗江永,祝春华,王力娜,杨燚,崔海瑛,季辉,张祥建. PI3-K/Akt通路在脑缺血治疗中的调控机制研究[J]. 脑与神经疾病杂志, 2013, 21(1): 45-48
作者姓名:苗江永  祝春华  王力娜  杨燚  崔海瑛  季辉  张祥建
作者单位:河北医科大学第二医院神经内科
摘    要:目的观察脑缺血-再灌注损伤后PI3-K/Akt通路的活性变化,并探讨阿利吉仑的调控机制。方法采用改良线栓法制备大脑中动脉缺血-再灌注模型。实验采用Western blot和qR-T PCR观察PI3-K、Akt基因和蛋白变化,比较各组脑梗死体积、患侧脑水肿和神经功能。结果缺血-再灌注后PI3-K、Akt表达明显减少。阿利吉仑通过激活PI3-K/Akt通路,明显改善神经功能缺失,减轻脑水肿,减小梗死体积。结论 PI3-K/Akt通路参与了阿利吉仑的脑保护作用,为其临床应用提供了理论基础。

关 键 词:脑缺血  磷脂酰肌醇-3羟基激酶  蛋白激酶B  阿利吉仑

The underling regulation mechanisms of PI3-K/Akt pathway activity in ischemia-reperfusion injury
MIAO Jiang-yong,ZHU Chun-hua,WANG Li-na,YANG Yi,CUI Hai-ying,JI Hui,ZHANG Xiang-jian. The underling regulation mechanisms of PI3-K/Akt pathway activity in ischemia-reperfusion injury[J]. Journal of Brain and Nervous Diseases, 2013, 21(1): 45-48
Authors:MIAO Jiang-yong  ZHU Chun-hua  WANG Li-na  YANG Yi  CUI Hai-ying  JI Hui  ZHANG Xiang-jian
Affiliation:.Department of Neurology,the Second Hospital of Hebei Medical University,Shijiazhuang 050000,China
Abstract:Objective This study is to evaluate PI3-K/Akt pathway activity in ischemia-reperfusion injury and explore the underling regulation mechanisms of aliskiren.Methods ICR mice were subjected to transient focal cerebral ischemia by right MCA occlusion.Aliskiren was systemically administered to explore the effect on PI3-K and Akt at 24 h after cerebral ischemia by western blot and qRT-PCR.The neurological deficits,brain water content and infarct volume were measured.Result Aliskiren dramatically up-regulated PI3-K and Akt,alleviated the neurological deficits,brain water content and infarct volumey.Conclusion PI3-K/Akt pathway is involved in the cerebral protective effects of aliskiren,providing a theoretical basis for its clinical application for cerebral ischemic therapies.
Keywords:Cerebral ischemia  Phosphatidylinositol 3-kinase  Serine-threonine kinase  Aliskiren
本文献已被 CNKI 等数据库收录!
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号