中文摘要：

目的：观察偏头痛大鼠造模测（右侧）三叉神经节大麻素受体1（CB1）、降钙素基因相关肽（CGRP）的表达和血清CGRP浓度,及电针干预对其影响,探讨电针在偏头痛中发挥镇痛效应的相关机制。方法：SD大鼠随机分为假手术组（A）、模型组（B）、模型＋电针组（C）、模型＋电针＋拮抗剂组（D）。电刺激右侧三叉神经节制作偏头痛模型。取“风池”“外关”电针治疗。QPCR和Western blot检测右测三叉神经节CB1/CGRP表达;ELISA检测血清CGRP浓度。结果：QPCR结果显示,CB1 m RNA表达：B组、C组、D组均明显高于A组（P〈0.05）;C组、D组均明显高于B组（P〈0.05）。CGRP m RNA表达：B组、C组、D组均明显高于A组（P〈0.05）;B组、D组均明显高于C组（P〈0.05）。Western blot结果显示：CB1蛋白表达：B组、C组、D组均明显高于A组（P〈0.05）;C组、D组均明显高于B组（P〈0.05）。CGRP蛋白表达：B组、C组、D组均明显高于A组（P〈0.05）;B组、D组均明显高于C组（P〈0.05）。血清CGRP浓度：针刺前B组、C组、D组明显高于A组（P〈0.05）;针刺5min及针刺10min后B组、C组、D组明显高于A组（P〈0.05）,B组、D组明显高于C组（P〈0.05）。结论：电针干预上调偏头痛大鼠三叉神经节CB1受体表达和下调三叉神经节CGRP表达,降低血清CGRP浓度,CB1拮抗剂可以部分拮抗电针对CGRP的影响。

英文摘要：

Objective： To observe the effect of electro-acupuncture （EA） intervention on expression of trigeminal ganglion CB 1 receptor, CGRP and serum concentrations of CGRP in migraine rats so as to study its mechanism underlying analgesic effect. Methods： Forty-eight Sprague Dawley rats were randomly divided into sham group （group A）, model group （group B） and EA group （group C）, and antagonist group （group D）. Migraine model was established by electrical stimulation of trigeminal ganglia. EA （2HZ/100HZ, lmA） was applied to dextral Fengchi （GB20）and Waiguan （SJ5） for 30min. The mRNA of CB1 and CGRP in fight trigeminal ganglionwas assayed using Q-PCR. Western blot method was adapted to measure protein expression of CB1 and CGRP. Serum concentration of CGRP was detected using ELISA. Results： Q-PCR and Western blot results showed that in comparison with group A, CB1 mRNA and protein expression of group B, group C and group D in fight trigeminal ganglia was significantly upregulated （P〈0.05）. Compared with group B, CB1 mRNA and protein expression of group C and group D in fight tfigeminal ganglia was remarkably upregulated （P〈0.05）. In comparison with group A, CGRP mRNA and protein expression of group B, group C and group D in right trigeminal ganglia was significantly upregulated （P〈0.05）. Compared with group C, CGRP mRNA and protein expression of group B and group D in fight trigeminal ganglia was upregulated （P〈0.05）. The outcomes of ELISA indicated that before EA and after EA for 5 min and 10 min, serum CGRP concentrations of group B, C, D were obviously higher than that of group A （P〈0.05）. After EA for 5 min and 10 min, CGRP concentrations of group B and group D were higher than that of group C （P〈0.05）. Conclusion： EA intervention could up-regulate CB1 receptor expression in trigeminal ganglion of migraine rat, down-regulate CGRP expression in trigeminal ganglia, and reduced serum concentrations of CGRP. CB 1 antagonist could partly compete th