Spinal Serotonin 1A Receptor Contributes to the Analgesia of Acupoint Catgut Embedding by Inhibiting Phosphorylation of the N-Methyl-D-Aspartate Receptor GluN1 Subunit in Complete Freund's Adjuvant-Induced Inflammatory Pain in Rats
Spinal Serotonin 1A Receptor Contributes to the Analgesia of Acupoint Catgut Embedding by Inhibiting Phosphorylation of the N-Methyl-D-Aspartate Receptor GluN1 Subunit in Complete Freund's Adjuvant-Induced Inflammatory Pain in Rats
复制标题
脊髓血清素 1A 受体通过抑制大鼠完全弗氏佐剂引起的炎症性疼痛中 N-甲基-d-天冬氨酸受体 GluN1 亚基的磷酸化，有助于穴位埋线的镇痛。
DOI：
10.1016/j.jpain.2018.07.011
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发表时间：
2019-01-01
期刊：
影响因子：
4
通讯作者：
Wang, Yan-Qing
中科院分区：
文献类型：
--
作者：
Cui, Wen-Qiang;Sun, Wen-Shan;Wang, Yan-Qing
穴位埋线（ACE）是一种广泛应用于治疗各种疾病的传统中医方法，包括慢性炎症性疼痛。我们试图评估ACE与电针（EA）可能的镇痛作用，并在大鼠后爪注射完全弗氏佐剂（CFA）诱导的炎症性疼痛模型中研究ACE的镇痛机制。采用von Frey、辐射热、步态分析等方法评价ACE和EA的镇痛作用，采用Western blot和免疫组化方法研究ACE的分子机制。ACE治疗每4天或每周在不同穴位（同侧、对侧或双侧ST36和GB30穴位）进行。减轻CFA注射引起的恶性反应最有效的ACE策略是每周一次在同侧ST36联合GB30进行ACE。同侧ST36和GB30每隔一天进行EA治疗，镇痛效果相当。ACE抑制了n -甲基-d -天冬氨酸受体GluN1亚基的激活增加和随后的Ca2+依赖信号（CaMKII， ERK和CREB），这些信号在CFA反应中发生。ACE的作用与鞘内注射维拉唑酮（一种5-羟色胺1A受体[5-HT1AR]激动剂）相似，并被WAY-100635（一种5-HT1AR拮抗剂）阻断。综上所述，我们发现ACE通过激活脊髓5-HT1AR和抑制GluN1的磷酸化，从而抑制Ca2+依赖性信号级联的激活，从而减轻cfa诱导的大鼠炎症性疼痛。展望：本文在cfa诱导的炎症性疼痛大鼠模型中，提供了ACE镇痛中脊髓5-HT1AR激活相关分子信号的新证据。这项工作可能有助于临床医生验证ACE镇痛的有效性，并更好地了解其潜在机制。(C) 2018年由美国疼痛学会发布。
Acupoint catgut embedding (ACE) is a widely used traditional Chinese medicine method to manage various diseases, including chronic inflammatory pain. We sought to assess the possible analgesic effects of ACE in comparison with electroacupuncture (EA) and to study the analgesic mechanisms of ACE in a rat model of inflammatory pain induced by injection of complete Freund's adjuvant (CFA) into the hind paw of rats. The von Frey, radiant heat, and gait analysis tests were performed to evaluate the analgesic effects of ACE and EA, and Western blot and immunohistochemistry assays were carried out to determine the molecular mechanisms of ACE. ACE treatments were administered every 4 days or every week with different acupoints (ipsilateral, contralateral, or bilateral ST36 and GB30 acupoints). The most effective ACE strategy for attenuating the nocifensive response induced by CFA injection was performing ACE once a week at ipsilateral ST36 in combination with GB30. EA treatment every other day at ipsilateral ST36 and GB30 showed comparable analgesic effects. ACE inhibited the increased activation of the GluN1 subunit of the N-methyl-D-aspartate receptor and the subsequent Ca2+-dependent signals (CaMKII, ERK, and CREB) that take place in response to CFA. The effects of ACE were similar to intrathecal injection of vilazodone (a serotonin 1A receptor [5-HT1AR] agonist) and were blocked by WAY-100635 (a 5-HT1AR antagonist). In summary, we show that ACE attenuates CFA-induced inflammatory pain in rats by activating spinal 5-HT1AR and by inhibiting the phosphorylation of GluN1, thus, inhibiting the activation of Ca2+-dependent signaling cascades.Perspective: This article presents the novel evidence concerning the spinal 5-HT1AR activation-related molecular signaling of ACE analgesia in a rat model of CFA-induced inflammatory pain. This work may help clinicians to verify the effectiveness of ACE analgesia and to better understand the underlying mechanism. (C) 2018 by the American Pain Society.