小胶质细胞
神经病理性疼痛
药理学
MAPK/ERK通路
痛觉过敏
医学
痛觉超敏
伤害
脊髓损伤
脊髓
前列腺素E2
超氧化物
止痛药
活性氧
化学
炎症
信号转导
受体
内分泌学
内科学
生物化学
酶
精神科
作者
Doo C. Choi,Jee Y. Lee,Eic Ju Lim,Hee Jung Baik,Tae Hwan Oh,Tae Young Yune
标识
DOI:10.1016/j.expneurol.2012.05.014
摘要
Acupuncture (AP) is currently used worldwide to relieve pain. However, little is known about its mechanisms of action. We found that after spinal cord injury (SCI), AP inhibited the production of superoxide anion (O2), which acted as a modulator for microglial activation, and the analgesic effect of AP was attributed to its anti-microglial activating action. Direct injection of a ROS scavenger inhibited SCI-induced NP. After contusion injury which induces the below-level neuropathic pain (NP), Shuigou and Yanglingquan acupoints were applied. AP relieved mechanical allodynia and thermal hyperalgesia, while vehicle and simulated AP did not. AP also decreased the proportion of activated microglia, and inhibited both p38MAPK and ERK activation in microglia at the L4–5. Also, the level of prostaglandin E2 (PGE2), which is produced via ERK signaling and mediates the below-level pain through PGE2 receptor, was reduced by AP. Injection of p38MAPK or ERK inhibitors attenuated NP and decreased PGE2 production. Furthermore, ROS produced after injury‐induced p38MAPK and ERK activation in microglia, and mediated mechanical allodynia and thermal hyperalgesia, which were inhibited by AP or a ROS scavenger. AP also inhibited the expression of inflammatory mediators. Therefore, our results suggest that the analgesic effect of AP may be partly mediated by inhibiting ROS-induced microglial activation and inflammatory responses after SCI and provide the possibility that AP can be used effectively as a non-pharmacological intervention for SCI-induced chronic NP in patients.
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