电针激活μ-阿片受体缓解大鼠痛情绪的机制  

The mechanism of electroacupuncture activating μ-opioid receptors to alleviate affective pain in rats

作　　者：郭霞[1] 杜振莹 郝娜 岳夏雅 王志华[2] 赵欣[1] 李建国[1] 张宇[1] Guo Xia;Du Zhenying;Hao Na;Yue Xiaya;Wang Zhihua;Zhao Xin;Li Jianguo;Zhang Yu(Department of Physiology and Key Laboratory for Cellular Physiology of Ministry of Education,Shanxi Medical University,Taiyuan 030001,China;Department of Pathology,Shanxi Medical University,Taiyuan 030001,China)

机构地区：[1]山西医科大学生理学系暨细胞生理学教育部重点实验室,太原030001 [2]山西医科大学病理学教研室,太原030001

出　　处：《神经解剖学杂志》2022年第5期507-513,共7页Chinese Journal of Neuroanatomy

基　　金：国家自然科学基金(81371254);山西省“1331工程”重点学科建设计划(XK201708)。

摘　　要：目的:探究电针(EA)通过激活μ-阿片受体(MOR)缓解大鼠痛情绪的机制。方法:预先在前扣带皮层喙侧部(rACC)分别注射生理盐水(NS)或MOR拮抗剂CTOP,并通过给大鼠左侧足底注射0.08 ml完全弗氏佐剂(CFA)建立条件位置逃避(CPA)模型,用电针(10 Hz,3 mA)或假电针(sham EA)刺激大鼠环跳穴(GB30)。行为测试完毕后,使用Western Blot检测rACC脑组织中的MOR蛋白表达以及N-甲基-D-天冬氨酸(NMDA)受体亚基2A和2B(NR2A和NR2B)的磷酸化水平。通过免疫荧光双标技术分别观察大鼠MOR和NR2A或NR2B的共表达情况。结果:与对照组比,注射CFA的大鼠第3 d在痛环境停留时间明显比第1 d缩短(P<0.05)并且rACC脑区p-NR2A、p-NR2B水平升高(P<0.01);电针治疗减少了CFA引起的逃避时间(P<0.05),增加了MOR的表达(P<0.01);在rACC给予CTOP后电针的作用被反转;免疫荧光结果显示在rACC脑区同一神经元上MOR分别与NR2A或NR2B共表达。结论:电针可能通过激活rACC脑区中的MOR下调p-NR2A和p-NR2B水平达到缓解CFA诱导痛情绪的效果。Objective:To investigate the mechanism of electroacupuncture(EA)alleviating the affective pain via activatingμ-opioid receptor(MOR)in rats.Methods:Normal saline(NS)or MOR antagonist CTOP were pre-injected into the rostral anterior cingulate cortex(rACC),conditioned place avoidance(CPA)model was established by injecting complete Freund adjuvant(CFA,0.08 ml)into the left hindpaw of rats,the rats’Huantiao acupoint(GB30)was stimulated with EA(10 Hz,3 mA)or sham EA.After behavioral test,the expression of MOR protein and the phosphorylation levels of N-methyl-D-aspartate(NMDA)receptor subunit 2 A and 2 B(NR2 A and NR2 B)in rACC were detected by Western Blot.The co-expression of MOR,NR2 A,and NR2 B was observed by immunofluorescence double labeling technique.Results:Compared with the control group,the time spent in the“pain environment”on day 3 was significantly shorter than that on day 1(P<0.05)and the phosphorylation levels of NR2 A and NR2 B in rACC increased(P<0.01)in CFA-injected rats;EA treatment reduced the avoidance time(P<0.05),and increased the expression of MOR(P<0.01);After administration of CTOP in rACC,the effect of EA was reversed;Immunofluorescence results showed that MOR was co-expressed with NR2 A or NR2 B in the same neuron,respectively.Conclusion:EA may activate MOR to downregulate the levels of p-NR2 A and p-NR2 B to alleviate CFA-induced affective pain.

关 键 词：疼痛 电针 前扣带皮层 Μ-阿片受体 大鼠 

分 类 号：R245.97[医药卫生—针灸推拿学]