中文摘要：

目的：探讨p38丝裂原活化蛋白激酶（MAPK）信号通路介导的炎性反应在电针防治帕金森病（Parkinsondisease，PD）模型大鼠中的作用。方法：健康雄性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。模型组与电针组大鼠采用颈背部皮下注射鱼藤酮（2mg／kg，溶解于葵花油，浓度2mg／mL）制备PD模型；假手术组，在与模型组大鼠相同部位注射等量的不合鱼藤酮的葵花油乳化液；正常组不作处理。电针组取“风府”“太冲”行电针治疗（连续波，频率2Hz，强度1mA，通电20min），1次／d，连续14d。其他组不予干预治疗。采用免疫组化法检测各组大鼠中脑黑质酪氨酸羟化酶（tyrosinehydroxylase，TH）、磷酸化p38丝裂原活化蛋白激酶（p—p38MAPK）、环氧合酶2（cyclOOxygenase-2，COX-2）的表达变化。结果：模型组大鼠出现典型的PD行为学改变，中脑黑质区TH阳性神经元计数较正常组、假手术组显著降低，P—p38MAPK、COX-2阳性神经元计数较正常组、假手术组显著升高，经统计学分析，差异均具有统计学意义（均P〈O．01）；电针组TH阳性神经元计数较模型组明显升高，p—p38MAPK、COX-2则较模型组表达下降，经统计学分析，差异均具有统计学意义（均P〈0．01）。结论：电针治疗可明显降低PD大鼠炎性介质COX-2的表达，抑制p38MAPK磷酸化，减轻PD大鼠多巴胺能神经元的损伤，这一作用可能与其影响p38MAPK信号通路有关。

英文摘要：

Objective To explore the role of inflammatory reaction mediated by p38-mitogen activated protein kinase （p38-MAPK） signal path on prevention and treatment of Parkinson disease （PD） model rats by electroacupuncture （EA）. Methods Thirty-two healthy male SD rats were randomly divided into a normal group, a sham operation group, a model group and an EA group, eight rats in each one. The PD model was established in the model group and EA group by subcutaneous injection of rotenone in skin-back area （2 mg/kg, dissolved in sun- flower oil, 2 mg/mL in density）, while the injection of sunflower oil emulsion without rotenone at the same point and quantity as the model group was applied in the sham operation group. The normal group was not given any in-tervention. The EA treatment （continuous wave, 2 Hz in frequency, 1 mA in intensity, 20 rain） was applied at ＂Fengfu＂ （GV 16） and ＂Taichong＂ （LR 3） in the EA group, once a day for continuously 14 days. No treatment was given in the other groups. The expression of tyrosine hydroxylase （TH）, phosphorylated p38-MAPK, cy- clooxygenase-2 （COX-2） in the substantia nigra were detected with immunohistochemical method. Results There was typical PD ethology change in the model group. Compared with the normal group and sham operation group, the expression of TH positive neuron in the substantia nigra in the model group was significantly decreased, while the expression of phosphorylated p38-MAPK and COX-2 were significantly increased （all P（0. 01）. Compared with the model group, the expression of TH positive neuron in the EA group was apparently increased, while the expressionof phosphorylated p38-MAPK and COX-2 were significantly decreased （all P〈0. 01）. Conclmion The EA therapy could obviously reduce the expression of inflammation mediator COX-2, inhibit the phosphorylation of p38-MAPK, reduce the damage of dopaminergic neurons in the rats with PD, and this effect may be related with the impact of p38-MAPK signal path.