[电针对帕金森病模型大鼠黑质细胞中p38丝裂原活化蛋白激酶的影响]

[Influence of electroacupuncture on p38-mitogen activated protein kinase in substantia nigra cells of rats with Parkinson disease model].

作者信息

Wang Shu-Ju, Fang Jian-Qiao, Ma Jun, Wang Yan-Chun, Zeng Xiao-Ling, Zhou Dan, Sun Guo-Jie

机构信息

Orthopedics Department of Hubei University of CM, Wuhan 430065, China.

出版信息

Zhongguo Zhen Jiu. 2013 Apr;33(4):329-33.

PMID:23819239

Abstract

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 sunflower 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 intervention. The EA treatment (continuous wave, 2 Hz in frequency, 1 mA in intensity, 20 min) 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, cyclooxygenase-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 expression of phosphorylated p38-MAPK and COX-2 were significantly decreased (all P < 0.01).

CONCLUSION

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

摘要

目的

探讨p38丝裂原活化蛋白激酶（p38-MAPK）信号通路介导的炎症反应在电针（EA）防治帕金森病（PD）模型大鼠中的作用。

方法

将32只健康雄性SD大鼠随机分为正常组、假手术组、模型组和EA组，每组8只。模型组和EA组通过在背部皮肤皮下注射鱼藤酮（2 mg/kg，溶于葵花籽油，浓度为2 mg/mL）建立PD模型，假手术组在相同部位和相同剂量注射不含鱼藤酮的葵花籽油乳剂。正常组不给予任何干预。EA组于“风府”（GV 16）和“太冲”（LR 3）穴行EA治疗（连续波，频率2 Hz，强度1 mA。持续20分钟），每天1次，连续14天。其他组不给予治疗。采用免疫组织化学方法检测黑质中酪氨酸羟化酶（TH）、磷酸化p38-MAPK、环氧合酶-2（COX-2）的表达。