电针治疗大鼠慢性炎症痛时脊髓环氧合酶-2 mRNA和蛋白的表达变化

Effects of Electroacupuncture on Chronic Inflammatory Pain and the Expression of Spinal Cyclooxygenase-2 mRNA and Protein

目的:观察多次电针对慢性炎症痛大鼠的镇痛作用和局部炎症组织的修复作用,以及对脊髓环氧合-酶2(cyclooxygenase-2,COX-2)mRNA和蛋白表达的影响。方法:SD雄性大鼠随机分为正常组、模型组和电针组,在佐剂性关节炎大鼠模型上,电针“阳陵泉”“昆仑”穴(频率2 Hz,强度≤1 mA,连续波,20 min/次,每天治疗1次)。用辐射热测痛法观察电针对慢性炎症痛大鼠辐射热痛敏分数的影响;用HE组织化学染色法观察电针对炎症组织的修复作用;用RT-PCR和免疫组织化学方法观察电针对慢性炎症痛大鼠脊髓COX-2 mRNA和蛋白表达的影响。结果:电针能显著减少慢性炎症痛大鼠痛敏分数的绝对值;电针治疗后大鼠关节腔内炎性渗出和滑膜中性粒细胞浸润基本消失,滑膜水肿减轻,滑膜囊表面修复;电针显著下调了炎症痛引起的大鼠脊髓COX-2 mRNA和蛋白的过度表达。结论:电针对慢性炎症痛大鼠有明显的镇痛作用;电针能较好地缓解局部炎症,促进炎症组织的修复;电针的镇痛作用可能与对脊髓COX-2 mRNA和蛋白表达的调节有关。

Objective： To observe the effects of electroacupuncture （EA） on hyperalgesia, inflarrrnatory tissue repair and the expression of spinal COX-2 mRNA and protein in rats with chronic inflammatory pain. Methods： Chronic inflammatory pain model was established by injection of complete Freund＇s adjuvant （CFA） into the SD rat＇s left ankle-joint cavity of the hind limb. EA （2 Hz, 1 mA, continuous waves） was applied to ＂Yanglingquan＂ （GB 34） and ＂Kunlun＂ （BL 60） for 20 min, once daily, continuously for 1 d, 4 d, 6 d, 8 d and 10 d respectively. For observing changes of tissue repair of the focus, HE staining technique was used; and for determining the expression of spinal COX-2 mRNA and COX-2 protein in the dorsal horns of the lumbar spinal cord, immunohistochemical and RT-PCR techniques were carried out. Results： After 6 days＇ EA treatment, the hyperalgesic score of EA group （n = 6） was significantly lower than that of model group （ n = 6） ; and after 8 and 10 days＇ treatment, the decreased hyperalgesic score of EA group was similar to that of control group （n = 6,P 〉 0.05）. Compared with model 1 （4 d after injection of CFA, n=3） and 2 （14 d after injection of CFA, n=3）, the exudation of the joint cavity, synovium edema, and infiltration of mononuclear cells of EA group （n=6） were improved remarkably. In comparison with control group, 4 days after injection of CFA, spinal COX-2 mRNA expression and COX-2 immuno-reaction positive cell number of model group increased significantly （ P〈 0.05）; 6 days after EA, no significant differences were found between control and EA groups in both COX-2 mRNA expression and COX-2 immuno-reaction positive cell number （ P 〉 0.05）, indicating that EA could down-regulate the expression of COX-2 mRNA and COX-2 protein in the spinal cord. Conclusion： EA has a remarkable analgesic effect and can promote the repair of inflammatory tissue, which may be related to its functions in down-regulating the expression of COX-2 mRNA and COX-2 protein in the spinal cord.