Wang Chao, Xie Wen-juan, Liu Mi, Yan Jie, Zhang Jia-li, Liu Zhao, Guo Li-na
Zhen Ci Yan Jiu. 2014 Oct;39(5):382-6.
To observe the effect of electroacupuncture (EA) intervention on changes of spinal a-amino-3- ydroxy-5-methylisoxazole-4-propionate acid (AMPA) receptor (GluR 1) expression in rats with chronic constrictive injury (CCI) pain, so as to explore its mechanisms underlying improvement of neuropathic pain.
Sixty male SD rats were randomly divided into sham-operation, CCI model and EA groups (n=20). Neuropathic pain model was established by ligature of the right sciatic nerve. EA stimulation (2 Hz, 1-3 mA) was applied to "Weizhong" (BL 40) and "Huantiao" (GB 30) on the injured limb for 30 min, once a day for 7 days beginning from the 11th day on after CCI. The mechanical and thermal pain thresholds were measured before and after the CCI procedure (baseline) and after EA intervention. The AMPA receptor subunit GluR 1 protein and gene expression in L5-L 6 segments of the spinal cord was detected using Western blot (WB), immunohistochemistry and re- verse transcription (RT)-polymerase chain reaction (PCR), separately.
As the results of mechanical and thermal pain thresholds in our past study, EA intervention could markedly raise CCl-reduced decreased pain threshold. Compared with the sham-operation group, the expression levels of spinal GluR 1 protein and mRNA in the model group were significantly increased (P<0.05, P<0.01). Following EA intervention, the expression levels of GluR 1 protein and mRNA were remarkably down-regulated in the EA group in comparison with those of the model group (all P<005).
EA intervention can down-regulate CCI-induced increase of AMPA receptor GIuR 1 expression in the lumbar spinal cord in CCI rats, which may contribute to its effect in alleviating neuropathic pain.
观察电针(EA)干预对慢性压迫性损伤(CCI)疼痛大鼠脊髓α-氨基-3-羟基-5-甲基异恶唑-4-丙酸(AMPA)受体(GluR 1)表达变化的影响,以探讨其改善神经病理性疼痛的机制。
将60只雄性SD大鼠随机分为假手术组、CCI模型组和EA组(n = 20)。通过结扎右侧坐骨神经建立神经病理性疼痛模型。从CCI术后第11天开始,对损伤肢体的“委中”(BL 40)和“环跳”(GB 30)进行EA刺激(2 Hz,1 - 3 mA),持续30分钟,每天1次,共7天。在CCI手术前(基线)和EA干预后测量机械性和热痛阈值。分别采用蛋白质免疫印迹法(WB)、免疫组织化学和逆转录(RT)-聚合酶链反应(PCR)检测脊髓L5 - L6节段AMPA受体亚基GluR 1蛋白和基因表达。
正如我们过去研究中机械性和热痛阈值的结果所示,EA干预可显著提高CCI降低的疼痛阈值。与假手术组相比,模型组脊髓GluR 1蛋白和mRNA表达水平显著升高(P < 0.05,P < 0.01)。EA干预后,与模型组相比,EA组GluR 1蛋白和mRNA表达水平显著下调(均P < 0.05)。
EA干预可下调CCI大鼠腰段脊髓中CCI诱导的AMPA受体GluR 1表达增加,这可能是其缓解神经病理性疼痛的作用机制。