Department of Integrative Medicine and Neurobiology, Institute of Acupuncture Research, State Key Laboratory of Medical Neurobiology, Institutes of Brain Science, Shanghai Medical College, Fudan University, Shanghai, China.
J Pain. 2011 Sep;12(9):974-84. doi: 10.1016/j.jpain.2011.03.002. Epub 2011 Jun 15.
Although electroacupuncture (EA) has been proven to effectively relieve pain associated with arthritis, the underlying mechanism of EA analgesia requires further investigation. Here, the involvement of spinal neurotrophin-3 (NT-3) in EA's analgesic effects on complete Freund's adjuvant (CFA)-induced inflammatory pain was examined. The present study demonstrated that: 1) repeated EA stimulation of ipsilateral GB30 and GB34 acupoints remarkably suppressed CFA-induced hyperalgesia; 2) EA treatment markedly enhanced the upregulation of spinal NT-3 mRNA and protein levels following CFA injection; 3) antisense oligodeoxynucleotides (ODN) specifically against NT-3 intrathecally administered during EA treatment for 7 days significantly attenuated the EA analgesia; and 4) the suppressed expression of spinal GFAP (astrocytic marker), OX-42 (microglial marker) as well as proinflammatory cytokines, interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α by EA treatment was significantly attenuated following NT-3 antisense ODN delivery. These results suggested that endogenous NT-3 may be involved in the analgesic effect of EA on inflammatory pain in rats, mediated through the inhibition of spinal glial activity as well as proinflammatory cytokine production.
The present study may initiate a discussion on the possible roles of NT-3/glia/cytokines in the therapeutic effects of acupuncture and provide insight on the mechanism underlie the analgesic effects of acupuncture on pain associated with arthritis.
虽然电针(EA)已被证明能有效缓解关节炎相关疼痛,但 EA 镇痛的潜在机制仍需进一步研究。在此,研究了脊髓神经营养因子-3(NT-3)在 EA 对抗完全弗氏佐剂(CFA)诱导的炎症性疼痛中的作用。本研究表明:1)同侧 GB30 和 GB34 穴位的重复 EA 刺激可显著抑制 CFA 引起的痛觉过敏;2)EA 治疗可显著增强 CFA 注射后脊髓 NT-3 mRNA 和蛋白水平的上调;3)EA 治疗期间鞘内给予 NT-3 反义寡核苷酸(ODN)可显著减弱 EA 镇痛作用;4)EA 治疗抑制脊髓 GFAP(星形胶质细胞标志物)、OX-42(小胶质细胞标志物)和促炎细胞因子白细胞介素(IL)-1β、IL-6 和肿瘤坏死因子(TNF)-α的表达,而给予 NT-3 反义 ODN 后则明显减弱。这些结果表明,内源性 NT-3 可能参与了 EA 对大鼠炎症性疼痛的镇痛作用,其机制可能是通过抑制脊髓胶质细胞活性和促炎细胞因子的产生。
本研究可能引发关于 NT-3/胶质细胞/细胞因子在针刺治疗作用中的可能作用的讨论,并为针刺治疗关节炎相关疼痛的镇痛作用机制提供新的见解。