Shou Yin, Zhao Ying-qian, Xu Ming-shu, Ge Lin-bao
Yueyang Hospital of Integrated Chinese and Western Shanghai University of Chinese Medicine, Shanghai 200437, China.
Zhen Ci Yan Jiu. 2011 Feb;36(1):18-22.
To observe the effect of repeated electroacupuncture (EA) on the expression of cannabinoid receptor-1 (CB 1) mrRNA and dopamine 1 receptor (D 1) mRNA in Nucleus Accumbens (NAC)-Caudate Nucleus (CN) region in inflammatory-pain rats, so as to study its underlying mechanism in analgesia.
A total of 30 SD rats were randomized into normal control, model, EA, EA+ AM 251 and WIN 55212-2 groups, with 6 cases in each group. EA (2 Hz/100 Hz, 1 -3 mA) was applied to "Zusanli"(ST 36) and "Kunlun"(BL 60) for 30 min, once every other day, and 4 sessions all together. Arthritis model was established by injection of Freund's complete adjuvant 0.05 mL in the rat's left ankle. Thermal pain threshold (paw withdrawal latency, PWL) was detected before and after modeling and after repeated EA and/or intraperitoneal injection of AM 251(an inverse antagonist at the CB 1 cannabinoid receptor, 0. 1 mg/100 g) and WIN 55212-2 (a potent cannabinoid receptor agonist, 0. 2 mg/100 g). The expression of CB 1 receptor mRNA and D 1 receptor mRNA in the NAC-CN region was measured by real time fluorescence quantitative-polymerase chain reaction.
Compared with the control group, the pain threshold values of the model group was decreased significantly (P<0.01). In comparison with the model group, the pain threshold values of the EA group and WIN 55212-2 group were increased considerably on day 10 (P<0. 01). No significant differences were found between the EA+ AM 251 and model groups and between the EA and WIN 55212-2 groups in PWL after the treatment (P>0.05). Compared with the control group, both CB 1 R mRNA and D 1 R mRNA expression levels in the model group were increased slightly, while in comparison with the model group and EA+ AM 251 group, CB 1 R mRNA and D 1 R mRNA expression levels in the EA group and WIN 55212-2 group were upregulated obviously. No significant differences were found between the EA + AM 251 and model groups and between the EA and WIN 55212-2 groups in CB 1 R mRNA and D 1 R mRNA expression levels.
观察重复电针（EA）对炎性疼痛大鼠伏隔核（NAC）-尾状核（CN）区域大麻素受体1（CB1）mRNA和多巴胺1受体（D1）mRNA表达的影响，以探讨其镇痛的潜在机制。
将30只SD大鼠随机分为正常对照组、模型组、电针组、电针+AM251组和WIN 55212-2组，每组6只。采用2Hz/100Hz、1-3mA的电针刺激“足三里”（ST 36）和“昆仑”（BL 60）30分钟，隔日1次，共4次。通过在大鼠左踝关节注射0.05mL弗氏完全佐剂建立关节炎模型。在建模前后以及重复电针和/或腹腔注射AM251（CB1大麻素受体反向拮抗剂，0.1mg/100g）和WIN 55212-2（强效大麻素受体激动剂，0.2mg/100g）后检测热痛阈值（足趾撤离潜伏期，PWL）。采用实时荧光定量聚合酶链反应检测NAC-CN区域CB1受体mRNA和D1受体mRNA的表达。
与对照组相比，模型组的痛阈值显著降低（P<0.01）。与模型组相比，电针组和WIN 55212-2组在第10天的痛阈值显著升高（P<0.01）。治疗后，电针+AM251组与模型组之间以及电针组与WIN 55212-2组之间的PWL无显著差异（P>0.05）。与对照组相比，模型组CB1R mRNA和D1R mRNA表达水平略有升高，而与模型组和电针+AM;251组相比，电针组和WIN 55212-2组CB1R mRNA和D1R mRNA表达水平明显上调。电针+AM251组与模型组之间以及电针组与WIN 55212-2组之间的CB1R mRNA和D1R mRNA表达水平无显著差异。
