电针结合天麻素对脑缺血大鼠海马CA3区BDNF与Nogo-A表达的调节作用

Effect of Electroacupuncture Combined with Gastrodin on the Expression of BDNF and Nogo-A in Hippocampal CA3 in Focal Cerebral Ischemia Rats

目的:研究电针结合天麻素对局灶性脑缺血大鼠海马CA3区脑源性神经生长因子(BDNF)与神经轴突生长抑制因子(Nogo-A)的表达是否有良性调节作用。方法:SD大鼠40只随机分为正常组、模型组、电针组、天麻素组和电针+天麻素组。采用线栓法阻塞大鼠右侧大脑中动脉复制局灶性脑缺血模型。造模成功后,按分组分别及同时给予电针刺激左侧"百会"、"足三里"穴,天麻素注射液腹腔注射。免疫组织化学SABC法检测BDNF和Nogo-A的表达。结果:与正常组相比,模型组大鼠缺血侧海马CA3区BDNF阳性神经元数量增加(P<0.05),Nogo-A阳性神经元数量增加(P<0.05);与模型组比较,电针组、天麻素组和电针+天麻素组大鼠缺血侧海马CA3区BDNF阳性神经元数量均显著增加(P<0.05),Nogo-A阳性神经元数量均减少(P<0.05);电针结合天麻素组BDNF阳性神经元数量较电针组、天麻素组增加(P<0.05),Nogo-A阳性神经元数量较电针组、天麻素组减少(P<0.05)。结论:电针结合天麻素对缺血侧海马CA3区BDNF的表达有上调作用,对Nogo-A的表达有下调作用,对脑缺血后有关受损神经功能的恢复可能起到良性的调节作用。

Objective：To study on electroacupuncture（EA）combined with gastrodin in hippocampal CA3 region of rats with focal cerebral ischemia（FCI）whether there is a benign regulatory role of BDNF and Nogo-A.Methods：Forty SD rats were randomly divided into normal,model,EA,gastrodin and EA＋gastrodin groups.FCI rats were induced by middle cerebral artery occlusion with thread embolus.EA was applied to left side＂Baihui＂and＂Zusanli＂,gastrodin was given to rats by intraperitoneal.The expressions of BDNF and Nogo-A in hippocampal CA3 detected by immunohistochemical.Results：Compared with normal group,the number of BDNF positive neurons increased（P〈0.05）,the number of Nogo-A positive neurons increased（P〈0.05）.Compared with model group,EA group,gastrodin group and EA＋gastrodin group,the number of BDNF positive neurons increased significantly（P〈0.05）,and the number of Nogo-A positive neurons decreased（P〈0.05）.Expression levels of BDNF in the EA＋gastrodin group increased significantly than the EA or gastrodin group（P〈0.05）,the expression of Nogo-A in the EA＋gastrodin group dncreased significantly than the EA or gastrodin group（P〈0.05）.Conclusion：EA combined with gastrodin have positive effect on the expression of BDNF in the hippocampal CA3 of the ischemic side was up-regulated,and the expression of Nogo-A was down regulated,which may play an important role in the recovery of the damaged nerve function after cerebral ischemia.