目的观察局灶性脑缺血再灌注损伤大鼠缺血半暗带NGF、P13K、Akt以及Bad蛋白的动态表达及脑络欣通(黄芪、川芎、三七、蜈蚣等)对其影响。方法以线栓法阻塞大鼠左侧大脑中动脉,复制局灶性脑缺血再灌注模型,缺血2h再灌注3、7、14d,用免疫组化染色SABC法分别检测缺血半暗带NGF、P13K、Akt、Bad的表达。结果与模型组相比,脑络欣通组在脑缺血再灌注3、7、14d后,能够明显增加P13K、Akt的表达(P〈0.01或P〈0.001);在再灌注7、14d,脑络欣通组NGF蛋白表达显著升高(P〈0.05或P〈0.01);再灌注14d,脑络欣通组Bad蛋白表达显著减少(P〈0.05)。结论脑络欣通能够保护脑缺血再灌注损伤大鼠脑组织,其作用机制可能与促进NGF表达,激活P13K/Akt通路并降低Bad蛋白表达有关。
AIM To observe the dynamic expressions of NGF, PI3K, Akt and Bad in the ischemic penumbra of rats with cerebral ischemia/reperfusion (I/R) and to study the role of Naoluo Xintong Decoction (Astragali Ra- dix, Chuanxiong Rhizoma, Notoginseng Radix et Rhizoma, Scolopendrap, etc. ) in the treatment. METHODS The model of I/R was induced by the intraluminal suture method, which made its left middle cerebral artery occlu- sion for two hours. Rats were randomly divided into 3 d group, 7 d group and 14 d group after ischemia reperfu- sion. Expressions of NGF, PI3K, Akt and Bad in ischemic penumbra were detected by SABC, respectively. RE- SULTS Expression index of PI3K and Akt in Naoluo Xintong Decoction (3 d, 7 d, 14 d) groups were higher than those in the model groups (P 〈0. 01 or P 〈0. 001 ). Protein expression index of NGF in Naoluo Xintong De- coction (7 d, 14 d) groups were higher than those in the model groups (P 〈0.05 or P 〈0.01 ), while protein ex- pression index of Bad in Naoluo Xintong Decoction ( 14 d) group were markedly lower ( P 〈 0.05 ). CONCLU- SION Naoluo Xintong Decoction can play a protective role in brain tissue damage induced by cerebral ischemia reperfusion. And their effcts might be correlated with enhancing the expression of NGF, activating the PI3K/Akt signaling pathway and down-regulating the expression of Bad protein.