电针对大鼠关节炎性痛的疗效观察及其脊髓机制探讨  

The Spinal Mechanism of Electroacupuncture on Inflammatory Pain

作　　者：王丽娜[1] 杨建平[1] 张育文[2] 李熳[2] 

机构地区：[1]苏州大学附属第一医院麻醉科,江苏苏州215006 [2]华中科技大学同济医学院神经生物学教研室,湖北武汉430030

出　　处：《苏州大学学报（医学版）》2006年第5期720-724,共5页Suzhou University Journal of Medical Science

基　　金：江苏省卫生厅科研基金资助项目(H200325);江苏省自然科学基金资助项目(BK2005033)

摘　　要：目的观察电针对大鼠关节炎性痛的疗效并探讨其脊髓机制。方法采用大鼠单侧佐剂性关节炎性痛模型,对大鼠致炎后14 d内的痛反应情况作连续记录,且观察致炎后不同时间段(分别取第37、d)脊髓后角西非单叶豆同工凝集素(BSI-B4)结合位点和N-甲基-D-天冬氨酸受体NR1亚型蛋白(NMDA,NR1)的表达情况,以及在针刺条件下上述指标的变化情况。结果(1)电针后能明显改善炎性痛组大鼠的各痛反应指标变化(P<0.01),但仍未恢复到生理盐水组水平。(2)注射后第3、7 d各组大鼠(包括第37、d组)脊髓背角的BSI-B4结合位点和NR1表达关系比较如下:炎性痛组表达明显高于生理盐水组(P<0.01);经电针治疗后,电针组表达较炎性痛组减弱,但仍然比生理盐水组高(P<0.01);炎性痛组和电针组大鼠NR1的表达还表现为3 d组>7 d组(P<0.01)。结论电针可以明显改善单侧佐剂性关节炎大鼠各类痛反应指标,其可能机制是通过减缓炎性痛大鼠C伤害性感受器的持久发放,以及下调脊髓后角浅层NR1的表达抑制兴奋性信息的传入,从而减缓痛觉过敏的形成达到治疗炎性痛的目的。Objective To observe the influence of electroacupuncture（EA） on inflammatory pain, and elucidate the changes of Banderaea simplicifolia Isolectin B4 （BSI-B4） binding sites and N-methyl- D-aspartate receptor one subunit （NMDAR-1） expression in the spinal cord following inflammatory pain. Methods In this study, we applied the complete Freunds＇ adjuvant （CFA）-induced inflammatory pain model, the aim was to elucidate the overall progression of inflammation within 14 days after injection of CFA . In addition, BSI-B4 binding sites and NMDAR-1 expression were detected in the spinal dorsal horn by using immuno-histochemistry following CFA-induced inflammation and EA treat- ment. Results （1） In general, intraplantar injection of 50μl CFA resulted in considerable changes in thermal hyperalgesia, edema of the hindpaw and ＂foot-bend＂ score by 5 h post-injection compared with baseline（ P 〈 0.01）. The changes could be significantly attenuated by EA treatment （P 〈 0.01）. （2） Both at the 3rd day and 7th day following injection, the mean immunoreactive area and optical density of NMDAR-1-LI and BSI-B4 labeled products in the inflammatory group were greater than that in the EA treatment group, the result in the latter were greater than that in the control group （all P〈0.01）. And in inflammatory group and EA treatment group, the expression of NMDAR-1 in the 3rd day group was also greater than that in the 7 th day group（ P % 0.05）. Conclusion The above data indicate that EA can reverse the inflammatory pain changes. Moreover, the mechanism is probably to down-regulation the NMDAR-1 expression in the superficial laminae of spinal dorsal horn and weaken the discharge of unmyelinated nociceptive afferent terminals which contribute significantly to the hyperalgesia.

关 键 词：N-甲基-D-天门冬氨酸 西非单叶豆同工凝集素 脊髓后角 电针 

分 类 号：R338.8[医药卫生—人体生理学] R245.97[医药卫生—基础医学]