电针对帕金森小鼠黑质致密部脑源性神经营养因子表达的影响

目的:探讨脑源性神经营养因子在电针促进帕金森小鼠黑质致密部突触可塑性中的作用。方法:24只C57BL/6J雄性小鼠,按照随机分组的原则分为空白组、空电组、模型组、电针组,每组6只。以腹腔注射(30 mg/kg)1-甲基-4苯基-1,2,3,6四氢吡啶诱导的帕金森小鼠作为研究对象,电针“合谷”“太冲”穴,频率2~100 Hz,电压2~4 V,疏密波,每日1次,每次20 min,7次为1疗程,共治疗3个疗程后,分别运用免疫组化和原位杂交检测脑源性神经营养因子及其mRNA表达。结果:模型组脑源性神经营养因子免疫组化阳性细胞计数、积分光密度较空白组、空电组减少,P<0.05;电针组阳性细胞计数、积分光密度增加,与模型组比较P<0.01。模型组脑源性神经营养因子mRNA原位杂交阳性细胞计数、积分光密度较空白组和空电组减少,P<0.01;电针组阳性细胞计数、积分光密度增加,与模型组比较P<0.05。结论:电针可促进帕金森小鼠黑质致密部脑源性神经营养因子及其mRNA的表达,从而促进帕金森小鼠突触可塑性作用的发挥。

Effect of Electroacupuncture on the Expression of BDNF and BDNF mRNA in Parkinson's Disease Mice

Objective: To observe the effect of electroacupuncture(EA) on the expression of brain-derived neurotrophic factor(BDNF) in substantia nigra compacta(SNC) of Parkinson's disease(PD) mice so as to study the synaptic plasticity.Methods: Twenty-four male mice(C57BL/6J) were averagely and randomly divided into normal control,EA,model and model EA groups.PD model was induced by injection(i.p.) of 1-methyl,4-phenyl-1,2,3,6 tetrahydropyridine((30 mg/kg)).EA((2-100 Hz),2-(4 V),dense-sparse waves) was applied to "Hegu"(LI 4) and "Taichong"(LR 3) for(20 min),once daily.After 21 treatments,the mice were killed for sampling SNC tissue which was then cut into sections for detecting the expression of BDNF and BDNF mRNA by immunohistochemical and in situ hybridization techniques respectively.Results: Both immunohistochemical and in situ hybridization assays showed that compared with normal control group,the number of BDNF and BDNF mRNA positive cells and integral optical density(OD) values of model group were significantly lower(P<0.05,0.01);compared with model group,the number of BDNF and BDNF mRNA positive cells and integral OD values in model EA group were significantly higher(P<0.05,0.01).No significant differences were found among normal control,EA and model EA groups in these indexes.Conclusion: EA can inhibit the down-regulation of expression of BDNF and BDNF mRNA of SNC in PD mice which maybe contribute to its effect in raising the synaptic plasticity of the degenerative dopaminergic neurons.