电针对鱼藤酮诱导的帕金森病模型大鼠黑质内ERK1/2及TNF-α的影响

Effect of electroacupuncture on ERK1/2 signaling pathway of substantia nigra cells of rotenone-induced rats model with Parkinson's disease

目的探讨电针对帕金森病(PD)模型大鼠黑质内ERK1/2信号通路及炎症因子肿瘤坏死因子(TNF)-α的作用及机制。方法雄性健康SD大鼠32只,随机分为正常组、假手术组、模型组、电针组,每组8只。模型组和电针组经颈背部注射鱼藤酮造模14 d,造模后进行行为学评价,电针组给予电针"风府"和"太冲"两穴治疗,连续治疗14 d;其余各组不做治疗,假手术组给予相同剂量的DMSO和生理盐水混合液。采用免疫组化法检测大鼠黑质区磷酸化的ERK1/2、酪氨酸羟化酶(TH)、TNF-α阳性细胞表达情况。结果各组大鼠神经行为学表现存在差异,与正常组、假手术组相比,模型组大鼠黑质区TH阳性细胞数减少(P<0.05),磷酸化的ERK1/2、TNF-α阳性细胞数增加(P<0.05);与模型组相比,电针组大鼠黑质区TH阳性细胞数增加(P<0.05),磷酸化的ERK1/2、TNF-α阳性细胞数减少(P<0.05)。结论电针可以通过调节PD模型大鼠体内MAPK/ERK1/2通路,降低p-ERK1/2在PD模型大鼠黑质区的表达,进而减少TNF-α的表达,对PD病的发生发展起到一定的调节作用。

Objective To observe the effect of electroacupuncture ( EA ) on ERK1/2 signaling pathway and inflammatory cytokines TNF-αin substantia nigra(SN)cells of rotenone-induced rats model with Parkinson''s disease(PD),and explore the mechanism of EA on PD . Methods A total of 32 male SD rats were randomly and averagely divided into normal ,sham-operation,model and EA groups.Model and EA groups were injected intradermally with rotenone ( dissolved in DMSO and saline in certain percentage ) on the nape of the neck for 14 d to establish PD model rats .Behavioral assessment was conducted after the establishment of PD rats model .EA group was applied to 'Fengfu'and'Taichong'points for 20 min once daily for 14 d.Other groups were not given treatments .After the treatments ,the rats were killed for sampling substantia nigra tissue to detect the number of TH ,p-ERK1/2 and TNF-αpositive cells by inmmuno-histochemistry .Results Rats in each group performed differently in neurobehavior .Compared with normal and sham-operation groups ,the expressions of TH positive cells were significantly reduced in model group (P<0.05),the expressions of p-ERK1/2 and TNF-αpositive cells were significantly increased in model group(P<0.05).Compared with that of model group,the expression of TH positive cells was significantly increased in EA group (P<0.05),the expressions of p-ERK1/2 and TNF-αpositive cells were significantly reduced in EA group (P<0.05).Conclusions EA therapy might reduce the expression of TNF-αin SN of PD rats by regulating the expression of p-ERK1/2(MAPK pathway),which might delay the process of PD.