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电针对 I 型复杂性区域疼痛综合征大鼠模型机械性痛觉过敏的缓解作用:通过抑制脊髓 CXCL12/CXCR4 信号传导。

Electroacupuncture Alleviates Mechanical Allodynia in a Rat Model of Complex Regional Pain Syndrome Type-I via Suppressing Spinal CXCL12/CXCR4 Signaling.

机构信息

Department of Neurobiology and Acupuncture Research, The Third Clinical Medical College, Zhejiang Chinese Medical University, Key Laboratory of Acupuncture and Neurology of Zhejiang Province, Hangzhou, 310053, China.

Department of Neurobiology and Acupuncture Research, The Third Clinical Medical College, Zhejiang Chinese Medical University, Key Laboratory of Acupuncture and Neurology of Zhejiang Province, Hangzhou, 310053, China.

出版信息

J Pain. 2020 Sep-Oct;21(9-10):1060-1074. doi: 10.1016/j.jpain.2020.01.007. Epub 2020 Jun 25.

Abstract

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.

摘要

复杂性区域疼痛综合征 (CRPS) 会导致患者出现慢性和剧痛。传统疗法效果不佳,使其成为最难治疗的神经疾病之一。电针 (EA) 是一种有效的替代疼痛缓解疗法。在这里,我们研究了 EA 是否对 CRPS Ⅰ 型 (CRPS-Ⅰ) 大鼠模型发挥镇痛作用及其相关机制。建立大鼠慢性缺血后疼痛 (CPIP) 模型来模拟 CRPS-Ⅰ。与 2 Hz EA 或假 EA 相比,100 Hz EA 对 CPIP 模型具有强大而持久的抗痛觉过敏作用。EA 显著抑制 CPIP 模型脊髓背角 (SCDH) 中 CXCL12/CXCR4 的过表达,导致 SCDH 中神经元和神经胶质细胞活性显著降低。药理学阻断 CXCR4 模拟了 EA 诱导的 SCDH 中的抗痛觉过敏作用和相关细胞事件,而外源性 CXCL12 则消除了 EA 的作用。CXCR4 信号导致 SCDH 中 ERK 激活,导致 CPIP 模型大鼠的机械性痛觉过敏,而 EA 则显著降低 ERK 激活。因此,我们证明 EA 干扰 SCDH 中的 CXCL12/CXCR4 信号及其下游 ERK 途径,对 CRPS-Ⅰ 动物模型发挥强大的抗痛觉过敏作用。我们的工作表明,EA 可能是临床治疗 CRPS-Ⅰ 的一种潜在治疗选择。观点:我们的工作确定,EA 通过抑制 CXCL12/CXCR4 信号通路对 CRPS-Ⅰ 动物模型发挥强大的抗痛觉过敏作用。EA 进一步减轻 SCDH 中神经元和神经胶质细胞的激活和 ERK 途径。这项工作表明,EA 可能是临床治疗 CRPS-Ⅰ 的一种潜在治疗选择。

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