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神经生长因子在与紧带相关的持续性肌肉疼痛大鼠模型中的作用。

Involvement of NGF in the rat model of persistent muscle pain associated with taut band.

机构信息

Department of Functional Anatomy and Neuroscience, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.

出版信息

J Pain. 2011 Oct;12(10):1059-68. doi: 10.1016/j.jpain.2011.04.010. Epub 2011 Jun 30.

Abstract

UNLABELLED

Myofascial pain syndrome (MPS) is an important clinical condition characterized by chronic muscle pain and a myofascial trigger point (MTrP) located in a taut band (TB). However, its pathogenic mechanism is still unclear. We developed an animal model relevant to conditions of MPS, and analyzed the mechanism of the muscle pain in this model. We applied eccentric contraction (EC) to a rat's gastrocnemius muscle (GM) for 2 weeks, and examined the mechanical withdrawal thresholds, histological changes, and expressions and contents of nerve growth factor (NGF). The mechanical withdrawal threshold decreased significantly at the next day of first EC and continued up to 9 days after EC. TBs were palpable at 3 to 8 days after initiation of EC. In EC animals, necrotic and regenerating muscle cells were found significantly more than in control animals. In EC animals, NGF expressions in regenerating muscle cells and NGF contents of GM were significantly higher than control animals. Administration of NGF receptor (TrkA) inhibitor K252a showed significant suppression of mechanical hyperalgesia in EC animals. Repeated EC induced persistent mechanical muscle hyperalgesia associated with TB. NGF expressed in regenerating muscle cells may have an important role in persistent mechanical muscle hyperalgesia which might be relevant to pathogenesis of MPS.

PERSPECTIVE

The present study shows that NGF expressed in regenerating muscle cells is involved in persistent muscular mechanical hyperalgesia. NGF-TrkA signaling in primary muscle afferent neurons may be one of the most important and promising targets for MPS.

摘要

未标记

肌筋膜疼痛综合征(MPS)是一种重要的临床病症,其特征为慢性肌肉疼痛和位于紧张带(TB)中的肌筋膜触发点(MTrP)。然而,其发病机制仍不清楚。我们建立了一种与 MPS 相关的动物模型,并分析了该模型中肌肉疼痛的机制。我们对大鼠的腓肠肌(GM)进行离心收缩(EC)2 周,并检测机械撤回阈值、组织学变化以及神经生长因子(NGF)的表达和含量。在首次 EC 的第二天,机械撤回阈值显著降低,并持续至 EC 后 9 天。在 EC 开始后 3 至 8 天,可触及 TB。在 EC 动物中,坏死和再生的肌肉细胞明显多于对照动物。在 EC 动物中,再生肌肉细胞中的 NGF 表达和 GM 中的 NGF 含量明显高于对照动物。给予 NGF 受体(TrkA)抑制剂 K252a 可显著抑制 EC 动物的机械性痛觉过敏。重复 EC 可引起持续的机械性肌肉痛觉过敏,并伴有 TB。再生肌肉细胞中表达的 NGF 可能在持续的机械性肌肉痛觉过敏中起重要作用,这可能与 MPS 的发病机制有关。

观点

本研究表明,再生肌肉细胞中表达的 NGF 参与了持续的肌肉机械性痛觉过敏。初级肌肉传入神经元中的 NGF-TrkA 信号可能是 MPS 最重要和最有前途的靶点之一。

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