电针治疗抑郁模型大鼠快速起效海马区BDNF-TrkB机制研究

目的:探讨电针抗抑郁治疗快速起效的海马神经元保护和发生机制。方法:SD大鼠32只随机分为正常组、模型组、药物组(盐酸氟西汀)和电针组,每组8只。采用孤养和长期中等强度未预知应激制备应激大鼠抑郁症模型,运用免疫组化法观察治疗7天时各组大鼠在海马CA1、CA3、DG各区BDNF及TrkB阳性神经元的表达。结果:①抑郁症模型存在海马区BDNF、TrkB表达下降,表现为阳性神经元平均灰度值上升、目标总面积下降;②治疗第7天,电针组海马神经元的BDNF及受体TrkB平均灰度值下降,且显著低于药物组,尤以CA3区为甚(P<0.01);③治疗第7天,电针组海马神经元的BDNF及受体TrkB阳性神经元总面积均明显升高,且明显高于药物组,以在DG区较为显著(P<0.05)。结论:电针能提高抑郁模型大鼠海马锥体神经细胞的生存、促进神经元再生;电针抗抑郁快速起效与BDNF、TrkB表达的迅速增加有关。

Rapid-effect Mechanism on BDNF-TrkB in Hippocampus of Depressive Model Rats by Electro-acupuncture

Objective：To explore the rapid antidepressant action and the protection mechanism of neurons in hippocampus by electro-acupuncture（EA）.Methods：32 SD rats were randomly divided into control,model,medication and EA group,8 in each group.Depressive model rats were replicated by chronic unpredicatable mild stress induction,and immunohistochemistry was used to observe the expression of BDNF and TrkB positive neurons at CA1,CA3 and DG of hippocampus in each group after 7 days treatment.Results：①In model group,the expression of BDNF and TrkB positive neurons in hippocampus decreased.It was embodied as the average gray value increased while the total objective area decreased.②After 7 days treatment,the average gray value of BDNF and TrkB positive neurons decreased in EA group,compared with meditation group,especially at CA3 of hippocampus（P0.01）.③After 7 days treatment,the total objective area of BDNF and TrkB positive neurons increased significantly in EA group,compared with meditation group,especially at DG of hippocampus（P0.05）.Conclusion：EA can maintain neuronal survival and stimulate neurogenesis in hippocampus;Antidepressant rapid-effect mechanism by EA may relate to the rapidly increased expression of BDNF and TrkB.