Chen Lin, Zhang Jing, Li Fan, Qiu Yue, Wang Lu, Li Ying-hua, Shi Jing, Pan Hui-Lin, Li Man
Department of Neurobiology, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Peoples Republic of China.
J Pain. 2009 Jul;10(7):732-9. doi: 10.1016/j.jpain.2008.12.012. Epub 2009 May 5.
Acupuncture is widely used clinically to treat acute and chronic pain conditions, but the mechanisms underlying its effect are not fully understood. Although endocannabinoids are involved in modulation of nociception in animal models and in humans, their role in acupuncture analgesia has not been assessed. In this report, we determined the effect of electroacupuncture (EA) on the level of anandamide in the skin tissue and the role of cannabinoid CB1 and CB2 receptors in the analgesic effect of EA in an animal model of inflammatory pain. Inflammatory pain was induced by local injection of complete Freund's adjuvant (CFA) into the hind paw of rats. Thermal hyperalgesia was tested with a radiant heat stimulus, and mechanical allodynia was quantified with von Frey filaments. The anandamide concentration in the skin tissue was measured by using high-performance liquid chromatography. EA, applied to GB30 and GB34, at 2 and 100Hz significantly reduced thermal hyperalgesia and mechanical allodynia induced by CFA injection. Compared with the sham group, EA significantly increased the anandamide level in the inflamed skin tissue. Local pretreatment with a specific CB2 receptor antagonist, AM630, significantly attenuated the antinociceptive effect of EA. However, the effect of EA was not significantly altered by AM251, a selective CB1 receptor antagonist. These findings suggest that EA potentiates the local release of endogenous anandamide from inflamed tissues. Activation of peripheral CB2 receptors contributes to the analgesic effect of EA on inflammatory pain.
This study shows that electroacupuncture increases the anandamide level in inflammatory skin tissues, and CB2 receptors contribute to the analgesic effect of electroacupuncture in a rat model of inflammatory pain. This information improves our understanding of the mechanisms involved in the analgesic effect of acupuncture.
针刺在临床上广泛用于治疗急慢性疼痛病症，但其作用机制尚未完全明确。尽管内源性大麻素参与动物模型和人体的痛觉调制，但它们在针刺镇痛中的作用尚未得到评估。在本报告中，我们在炎症性疼痛动物模型中确定了电针（EA）对皮肤组织中花生四烯乙醇胺水平的影响以及大麻素CB1和CB2受体在EA镇痛作用中的作用。通过向大鼠后爪局部注射完全弗氏佐剂（CFA）诱导炎症性疼痛。用辐射热刺激测试热痛觉过敏，用von Frey细丝量化机械性异常性疼痛。使用高效液相色谱法测量皮肤组织中的花生四烯乙醇胺浓度。施加于GB30和GB34的2Hz和100Hz电针显著减轻了CFA注射诱导的热痛觉过敏和机械性异常性疼痛。与假手术组相比，电针显著提高了炎症皮肤组织中的花生四烯乙醇胺水平。用特异性CB2受体拮抗剂AM630进行局部预处理可显著减弱电针的抗伤害感受作用。然而，选择性CB1受体拮抗剂AM251并未显著改变电针的作用效果。这些发现表明，电针可增强炎症组织中内源性花生四烯乙醇胺的局部释放。外周CB2受体的激活有助于电针对炎症性疼痛的镇痛作用。
本研究表明，电针可提高炎症性皮肤组织中的花生四烯乙醇胺水平，且CB2受体有助于电针在炎症性疼痛大鼠模型中的镇痛作用。这一信息增进了我们对针刺镇痛作用机制的理解。
