| 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.PI3K/Akt 通路在电针预处理诱导脑缺血耐受中的机制研究[J].,2012,12(7):1215-1218 |
| PI3K/Akt 通路在电针预处理诱导脑缺血耐受中的机制研究 |
| Electroacupuncture Preconditioning Attenuate Focal CerebralIschemia-Reperfusion Injury Through PI3K/Akt Signal Pathway in Rats |
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| DOI： |
| 中文关键词: 电针 预处理 脑保护 PI3K/Akt 通路 |
| 英文关键词: Electroacpuncture Brain Ischemia reperfusion Preconditioning |
| 基金项目:国家自然科学基金项目（81028006；81173394） |
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| 中文摘要: |
| 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Akt（Ser473）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。 |
| 英文摘要: |
| Objective: To investigate the role of PI3K/Akt signal pathway in electroacupuncture preconditioning against focal
cerebral ischemia-reperfusion injury in rats. Methods: Focal cerebral ischemia was induced by middle cerebral artery occlusion using the
intraluminal filament technique in male rats. Brain ischemic injury was evaluated by neurologic scores, infarction volumes. What's more,
the expression of pAkt were examined by Western blotting. Results: Electroacupuncture improved neurologic outcome, reduced infarct
size as well as up-regulated the expression of pAkt at the early phase of reperfusion. Pretreatment with LY294002 completely reversed
the protection of EA against cerebral reperfusion injury. Conclusion: Up regulation of pAkt expression induced by activation of PI3K/Akt
signal pathway is involved in the protective effect of electroacupuncture preconditioning against focal cerebral I/R injury in rats. |
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