TRPV1型
背根神经节
腺苷
小胶质细胞
药理学
腺苷受体
受体
医学
痛觉过敏
类阿片
伤害感受器
瞬时受体电位通道
胶质纤维酸性蛋白
神经病理性疼痛
电针
导航1
炎症
伤害
脊髓
化学
吗啡
神经炎症
内科学
内分泌学
针灸科
病理
兴奋剂
替代医学
免疫组织化学
精神科
作者
Hsien-Tzung Liao,Ching Liang Hsieh,Chun Ming Huang,Yi Lin
摘要
Abstract 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 6 -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.
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