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Role of Sigma-1 Receptor/p38 MAPK Inhibition in Acupoint Catgut Embedding–Mediated Analgesic Effects in Complete Freund’s Adjuvant-Induced Inflammatory Pain
背景与目的
内质网伴侣蛋白Sigma-1受体（Sig-1R）和丝裂原活化蛋白激酶（MAPKs）参与疼痛的致病机制。穴位刺激在炎性疼痛中发挥抗痛觉过敏作用。然而，Sig-1 R和MAPKs是否与穴位刺激诱发的镇痛作用相关联尚不清楚。本研究探讨了穴位埋线（ACE）的镇痛作用以及抑制Sig-1 R和MAPKs在穴位埋线镇痛中的作用。
方 法
大鼠鞘内植入导管，穴位埋线应用于大鼠炎性疼痛模型（完全弗氏佐剂[CFA]椎间盘内注射）。双侧“昆仑”（BL60），“足三里”（ST36）和“三阴交”（SP6）穴位，鞘内每天给予Sig-1R激动剂PRE084或盐水。在完全弗氏佐剂注射前和完全弗氏佐剂注射后1,3和5天测量爪退缩阈值和爪水肿。并在完全弗氏佐剂注射后1,3和5天，采用Western bolt检测脊髓Sig-1R，p38MAPK和细胞外信号调节激酶（ERK）的蛋白表达水平以及采用免疫组织化学检测Sig-1。
结 果
穴位埋线表现出特异性的止痛作用。穴位埋线增加爪退缩阈值，并在1,3和5天显著降低完全弗氏佐剂诱发的爪水肿。穴位埋线降低Sig-1R的蛋白表达，其在注射完全弗氏佐剂后1,3和5天显著增加。穴位埋线在第1天和3天降低p38 MAPK和ERK的表达，第5天并不降低p38 MAPK和ERK的表达。然而，注射Sig-1R激动剂PRE084显著逆转了这些改变，除了不改变ERK表达。
结 论
本研究表明在完全弗氏佐剂诱发的炎性疼痛模型中，穴位埋线表现出抗痛觉过敏作用，其通过抑制Sig-1R降低p38 MAPK的表达，但不改变ERK的表达，发挥抗痛觉过敏的作用。
原始文献摘要
Du K,Wang X，Chi L,et al.Role of Sigma-1 Receptor/p38 MAPK Inhibition in Acupoint Catgut Embedding–Mediated Analgesic Effects in Complete Freund’s Adjuvant-Induced Inflammatory Pain.Anesth Analg.2017 Aug;125(2):662-669. doi: 10.1213/ANE.0000000000001857.
Abstract
BACKGROUND: The endoplasmic reticulum chaperone protein Sigma-1 receptor (Sig-1 R) and mitogen-activated protein kinases (MAPKs) are involved in the mechanism of pain.Acupoint stimulation exerts an exact antihyperalgesic effect in inflammatory pain.However,whether Sig-1R and MAPKs are associated with the acupoint stimulation-induced analgesic effects is not clear.This study investigated the analgesic effect of acupoint catgut embedding (ACE) and the inhibition of Sig-1 R and MAPKs in ACE analgesia.
METHODS: Rats were prepared with intrathecal catheter implantation.ACE was applied to bilateral“Kunlun”(BL60),“Zusanli”(ST36),and “Sanyinjiao”(SP6) acupoints in the rat model of inflammatory pain (complete Freund’s adjuvant [CFA] intraplantar injection).Then,Sig-1R
agonist PRE084 or saline was intrathecally given daily.The paw withdrawal thresholds and paw edema were measured before CFA injection and at 1,3, and 5 day after CFA injection.Western bolt was used to evaluate the protein expression of spinal Sig-1R,p38MAPK,and extracellular Signal-regulated kinase (ERK),and immunohistochemistry of Sig-1R was detected at 1, 3, and 5 days after CFA injection.
RESULTS: ACE exhibited specific analgesic effects.ACE increased paw withdrawal thresholds and markedly decreased CFA-induced paw edema at 1, 3,and 5 days.ACE downregulated the protein expression of Sig-1R,which was increased significantly at 1,3,and 5 days after CFA injection.ACE decreased the expression of p38 MAPK and ERK at 1 and 3 days but not at 5 days.However,an injection of Sig-1R agonist PRE084 markedly reversed these alterations,except ERK expression.
CONCLUSIONS: The present study demonstrated that ACE exhibited antihyperalgesic effects via the inhibition of the Sig-1R that modulated p38 MAPK,but not ERK, expression in the CFAinduced inflammatory pain model in rats.
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