Electroacupuncture Alleviates Mechanical Allodynia in a Rat Model of Complex Regional Pain Syndrome Type-I via Suppressing Spinal CXCL12/CXCR4 Signaling
Electroacupuncture Alleviates Mechanical Allodynia in a Rat Model of Complex Regional Pain Syndrome Type-I via Suppressing Spinal CXCL12/CXCR4 Signaling
复制标题
电针通过抑制脊髓 CXCL12/CXCR4 信号传导减轻 I 型复杂区域疼痛综合征大鼠模型中的机械异常性疼痛
DOI：
10.1016/j.jpain.2020.01.007
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发表时间：
2020-09-01
期刊：
影响因子：
4
通讯作者：
Liu, Boyi
中科院分区：
文献类型：
--
作者：
Hu, Qimiao;Zheng, Xiaoli;Liu, Boyi
复杂性区域疼痛综合征（CRPS）导致患者的慢性和难以忍受的疼痛。传统疗法缺乏有效性，使其成为最难治疗的神经系统疾病之一。电针是一种有效的镇痛替代疗法。本研究旨在探讨电针对大鼠CRPS-I模型的镇痛作用及其机制。建立大鼠慢性缺血后疼痛（CPIP）模型，模拟CRPS-I。100 Hz电针对CPIP模型的镇痛作用强于2 Hz电针或假电针。电针可明显抑制CPIP模型脊髓背角CXCL 12/CXCR 4的过度表达，导致脊髓背角神经元和胶质细胞活性显著降低。药理学阻断CXCR 4模拟EA诱导的SCDH的抗异常性疼痛作用和相关的细胞事件，而外源性CXCL 12取消EA的作用。CXCR 4信号通路导致SCDH中ERK的激活，导致CPIP模型大鼠的机械性异常性疼痛，而EA显著降低ERK的激活。因此，我们证明了EA干扰SCDH和下游ERK通路中的CXCL 12/CXCR 4信号传导，以在CRPS-I动物模型上发挥稳健的抗异常性疼痛作用。我们的工作表明，EA可能是一个潜在的治疗选择CRPS-I在clinic.Perspective：我们的工作确定，EA发挥强大的抗异常性疼痛作用的CRPS-I的动物模型，通过涉及抑制CXCL 12/CXCR 4信号传导的机制。EA进一步减弱SCDH中下游神经元和神经胶质细胞活化和ERK通路。这项工作表明，EA可能是一个潜在的治疗选择CRPS-I管理在临床上。(c)美国疼痛研究协会（United States Association for the Study of Pain，Inc.）
Complex regional pain syndrome (CRPS) results in chronic and excruciating pain in patients. Conventional therapies lack effectiveness, rendering it one of the most difficult to treat neurological conditions.. Electroacupuncture (EA) is an effective alternative therapy for pain relief. Here, we investigated whether EA exerts analgesic effect on a rat model of CRPS type-I (CRPS-I) and related mechanisms. The rat chronic postischemic pain (CPIP) model was established to mimic CRPS-I. 100Hz EA exerted robust and persistent antiallodynic effect on CPIP model compared with 2 Hz EA or sham EA. EA markedly suppressed the overexpression of CXCL12/CXCR4 in spinal cord dorsal horn (SCDH) of CPIP model, leading to substantial decrease in neuronal and glial cell activities in SCDH. Pharmacological blocking CXCR4 mimicked EA-induced antiallodynic effect and related cellular events in SCDH, whereas exogenous CXCL12 abolished EA's effect. CXCR4 signaling resulted in ERK activation in SCDH, contributing to mechanical allodynia of CPIP model rats, whereas EA markedly reduced ERK activation. Therefore, we demonstrated that EA interferes with CXCL12/CXCR4 signaling in SCDH and downstream ERK pathway to exert robust antiallodynic effect on an animal model of CRPS-I. Our work suggests that EA may be a potential therapeutic option for CRPS-I in clinic.Perspective: Our work identified that EA exerts robust antiallodynic effect on an animal model of CRPS-I, via mechanisms involving inhibition of CXCL12/CXCR4 signaling. EA further attenuates downstream neuronal and glial cell activation and ERK pathway in SCDH. This work suggests that EA may be a potential therapeutic option for CRPS-I management in clinic. (c) 2020 by United States Association for the Study of Pain, Inc.