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肉毒杆菌神经毒素A在神经性疼痛模型中的抗痛觉过敏疗效。

Anti-allodynic efficacy of botulinum neurotoxin A in a model of neuropathic pain.

作者信息

Luvisetto S, Marinelli S, Cobianchi S, Pavone F

机构信息

CNR Institute of Neuroscience, Psychobiology and Psychopharmacology, Via del Fosso di Fiorano 64, I-00143 Roma, Italy.

出版信息

Neuroscience. 2007 Mar 2;145(1):1-4. doi: 10.1016/j.neuroscience.2006.12.004. Epub 2007 Jan 9.

DOI:10.1016/j.neuroscience.2006.12.004
PMID:17218063
Abstract

Neuropathic pain is typified by injuries to the peripheral and central nervous system and derives from such causes as cancer, diabetes, multiple sclerosis, post-herpetic neuralgia, physical trauma or surgery, and many others. Patients suffering neuropathic pain do not respond to conventional treatment with non-steroidal anti-inflammatory drugs and show a reduced sensitivity to opiates often associated with serious side effects. Recently, it has been demonstrated that botulinum neurotoxin serotype-A (BoNT/A) is able to induce analgesia in inflammatory pain conditions. The goal of this research was to test if BoNT/A was able to relieve also neuropathic pain symptoms. By using chronic constriction injury of the sciatic nerve, a mouse model of neuropathic pain, we observed that peripheral administration of BoNT/A strongly reduced the mechanical allodynia associated with this neuropathy. Remarkably, a single non-toxic dose of BoNT/A was sufficient to induce anti-allodynic effects, which lasted for at least 3 weeks. This result is particularly relevant since neuropathic pain is poorly treated by current drug therapies. This communication enlarges our knowledge on potentially new medical uses of BoNT/A in efforts to ameliorate human health conditions, with very important implications in the development of new pharmacotherapeutic approaches against neuropathic pain.

摘要

神经性疼痛以周围和中枢神经系统损伤为典型特征,其病因包括癌症、糖尿病、多发性硬化症、疱疹后神经痛、身体创伤或手术等诸多因素。患有神经性疼痛的患者对非甾体抗炎药的传统治疗无反应,且对通常伴有严重副作用的阿片类药物敏感性降低。最近,已证明A型肉毒杆菌神经毒素(BoNT/A)在炎性疼痛情况下能够诱导镇痛作用。本研究的目的是测试BoNT/A是否也能够缓解神经性疼痛症状。通过使用坐骨神经慢性压迫损伤这一神经性疼痛小鼠模型,我们观察到外周给予BoNT/A可显著减轻与该神经病变相关的机械性异常性疼痛。值得注意的是,单次无毒剂量的BoNT/A足以诱导抗异常性疼痛效应,且该效应持续至少3周。鉴于目前的药物疗法对神经性疼痛治疗效果不佳,这一结果尤为重要。本通讯扩展了我们对BoNT/A潜在新医学用途的认识,有助于改善人类健康状况,对开发治疗神经性疼痛的新药物治疗方法具有非常重要的意义。

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