PI3-K/Akt通路在脑缺血治疗中的调控机制研究

被引：3

作者：

苗江永

祝春华

王力娜

杨燚

崔海瑛

季辉

张祥建

机构：

[1] 河北医科大学第二医院神经内科

来源：

脑与神经疾病杂志 | 2013年 / 01期

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;

D O I：

暂无

中图分类号：

R743.32 [脑血栓形成];

学科分类号：

1002 ;

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。

引用

页码：45 / 48

页数：4

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