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。
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.
出处
《现代生物医学进展》
CAS
2012年第7期1215-1218,共4页
Progress in Modern Biomedicine
基金
国家自然科学基金项目(81028006
81173394)
