PI3K/Akt通路在电针预处理诱导脑缺血耐受中的机制研究

被引：12

作者：

何二涛 ^{[1
]}

张霞婧 ^{[1
]}

马磊 ^{[1
]}

朱萧玲 ^{[1
]}

王强 ^{[1
]}

曹丽 ^{[1
]}

李丽 ^{[1
]}

赵宁侠 ^{[2
]}

左志义 ^{[3
]}

陈绍洋 ^{[1
]}

机构：

[1] 第四军医大学西京医院麻醉科

[2] 第四军医大学唐都医院中医科

[3] Department of Anesthesiology University of

来源：

现代生物医学进展 | 2012年 / 12卷 / 07期

关键词：

电针; 预处理; 脑保护; PI3K/Akt通路;

D O I：

10.13241/j.cnki.pmb.2012.07.042

中图分类号：

R743.3 [急性脑血管疾病（中风）];

学科分类号：

摘要：

目的:通过观察电针预处理对磷脂酰肌醇3激酶/蛋白质丝氨酸苏氨酸激酶(PI3K/Akt)通路的变化以及该通路抑制剂对电针预处理的脑保护的影响,探讨电针预处理诱导脑缺血耐受的可能机制。方法:线栓法单侧阻断大脑中动脉120min,再灌注24h制备大鼠大脑局灶性缺血再灌注(I/R)模型;Western Blot检测Akt磷酸化水平的变化;侧脑室注射PI3K/Akt通路抑制剂LY294002;神经行为学评分(Garcia标准)及TTC染色检测脑梗死体积比评价脑损伤程度。结果:电针预处理使大鼠神经行为学评分增高,脑梗死体积比降低(P<0.05);可上调Akt磷酸化水平,I/R2h达高峰(P<0.05)。侧脑室注射PI3K/Akt抑制剂LY294002,拮抗电针预处理的脑保护作用(P<0.05)。结论:电针预处理增加Ak(tSer473)磷酸化水平,在缺血再灌注早期上调PI3K/Akt通路可能是诱导大鼠脑缺血耐受的产生的主要机制。

引用

页码：1215 / 1218

页数：4

共 11 条

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