College of Chinese Medicine, Graduate Institute of Acupuncture Science, China Medical University, Taichung 40402, Taiwan.
Department of Acupuncture, China Medical University Hospital, Taichung 40402, Taiwan.
Sci Rep. 2017 Feb 13;7:42531. doi: 10.1038/srep42531.
Pain is associated with several conditions, such as inflammation, that result from altered peripheral nerve properties. Electroacupuncture (EA) is a common Chinese clinical medical technology used for pain management. Using an inflammatory pain mouse model, we investigated the effects of EA on the regulation of neurons, microglia, and related molecules. Complete Freund's adjuvant (CFA) injections produced a significant mechanical and thermal hyperalgesia that was reversed by EA or a transient receptor potential V1 (TRPV1) gene deletion. The expression of the astrocytic marker glial fibrillary acidic protein (GFAP), the microglial marker Iba-1, S100B, receptor for advanced glycation end-products (RAGE), TRPV1, and other related molecules was dramatically increased in the dorsal root ganglion (DRG) and spinal cord dorsal horn (SCDH) of CFA-treated mice. This effect was reversed by EA and TRPV1 gene deletion. In addition, endomorphin (EM) and N-cyclopentyladenosine (CPA) administration reliably reduced mechanical and thermal hyperalgesia, thereby suggesting the involvement of opioid and adenosine receptors. Furthermore, blocking of opioid and adenosine A1 receptors reversed the analgesic effects of EA. Our study illustrates the substantial therapeutic effects of EA against inflammatory pain and provides a novel and detailed mechanism underlying EA-mediated analgesia via neuronal and non-neuronal pathways.
疼痛与多种疾病相关，例如炎症，这些疾病源于外周神经特性的改变。电针（EA）是一种常用于疼痛管理的常见中医临床医疗技术。我们使用炎性疼痛小鼠模型，研究了 EA 对神经元、小胶质细胞和相关分子的调节作用。完全弗氏佐剂（CFA）注射会引起明显的机械性和热痛觉过敏，这种过敏可以通过 EA 或瞬时受体电位 V1（TRPV1）基因缺失来逆转。在 CFA 处理的小鼠的背根神经节（DRG）和脊髓背角（SCDH）中，星形胶质细胞标志物胶质纤维酸性蛋白（GFAP）、小胶质细胞标志物 Iba-1、S100B、晚期糖基化终产物受体（RAGE）、TRPV1 和其他相关分子的表达显著增加。这种效应可以通过 EA 和 TRPV1 基因缺失来逆转。此外，内吗啡肽（EM）和 N-环戊基腺苷（CPA）的给药可靠地减轻了机械性和热痛觉过敏，从而表明阿片类和腺苷受体的参与。此外，阿片类和腺苷 A1 受体的阻断逆转了 EA 的镇痛作用。我们的研究说明了 EA 对炎性疼痛的显著治疗效果，并提供了 EA 通过神经元和非神经元途径介导镇痛的新的详细机制。
