CAJ | 학술논문

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ERK12／、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。
목적：탐토전침대파금삼병（PD）모형대서흑질내ERK1／2신호통로급염증인자종류배사인자（TNF）－α적작용급궤제。방법웅성건강SD대서32지，수궤분위정상조、가수술조、모형조、전침조，매조8지。모형조화전침조경경배부주사어등동조모14 d，조모후진행행위학평개，전침조급여전침“풍부”화“태충”량혈치료，련속치료14 d；기여각조불주치료，가수술조급여상동제량적 DMSO화생리염수혼합액。채용면역조화법검측대서흑질구린산화적ERK1／2、락안산간화매（ TH）、TNF－α양성세포표체정황。결과각조대서신경행위학표현존재차이，여정상조、가수술조상비，모형조대서흑질구TH양성세포수감소（P＜0．05），린산화적ERK12／、TNF－α양성세포수증가（P＜0．05）；여모형조상비，전침조대서흑질구TH양성세포수증가（ P＜0．05），린산화적 ERK1／2、TNF－α양성세포수감소（ P＜0．05）。결론전침가이통과조절 PD 모형대서체내 MAPK／ERK1／2통로，강저p－ERK1／2재PD모형대서흑질구적표체，진이감소TNF－α적표체，대PD병적발생발전기도일정적조절작용。
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.