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本文引用的文献

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Role of MAPKs in platinum-induced neuronal apoptosis.丝裂原活化蛋白激酶(MAPKs)在铂诱导的神经元凋亡中的作用。
Neurotoxicology. 2009 Mar;30(2):312-9. doi: 10.1016/j.neuro.2009.01.003. Epub 2009 Jan 21.
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TrkB signaling is required for both the induction and maintenance of tissue and nerve injury-induced persistent pain.TrkB信号传导对于组织损伤和神经损伤诱导的持续性疼痛的诱导和维持均是必需的。
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Central pain in multiple sclerosis - sensory abnormalities.多发性硬化症中的中枢性疼痛——感觉异常。
Eur J Pain. 2010 Jan;14(1):104-10. doi: 10.1016/j.ejpain.2009.03.003. Epub 2009 Apr 8.
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Herpes zoster (shingles) and postherpetic neuralgia.带状疱疹(蛇串疮)及带状疱疹后神经痛。
Mayo Clin Proc. 2009 Mar;84(3):274-80. doi: 10.4065/84.3.274.
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Acetyl-l-carnitine and nucleoside reverse transcriptase inhibitor-associated neuropathy in HIV infection.乙酰左旋肉碱与HIV感染中核苷类逆转录酶抑制剂相关的神经病变
HIV Med. 2009 Feb;10(2):103-10. doi: 10.1111/j.1468-1293.2008.00658.x.
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Oxidant-induced changes in mitochondria and calcium dynamics in the pathophysiology of Alzheimer's disease.氧化应激诱导的线粒体变化及钙动力学在阿尔茨海默病病理生理学中的作用
Ann N Y Acad Sci. 2008 Dec;1147:221-32. doi: 10.1196/annals.1427.038.
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Human immunodeficiency virus protease inhibitors and risk for peripheral neuropathy.人类免疫缺陷病毒蛋白酶抑制剂与周围神经病变风险
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Tubulin binding blocks mitochondrial voltage-dependent anion channel and regulates respiration.微管蛋白结合可阻断线粒体电压依赖性阴离子通道并调节呼吸作用。
Proc Natl Acad Sci U S A. 2008 Dec 2;105(48):18746-51. doi: 10.1073/pnas.0806303105. Epub 2008 Nov 24.
9
Acetyl-L-carnitine provides effective in vivo neuroprotection over 3,4-methylenedioximethamphetamine-induced mitochondrial neurotoxicity in the adolescent rat brain.乙酰左旋肉碱对青少年大鼠大脑中3,4-亚甲基二氧甲基苯丙胺诱导的线粒体神经毒性具有有效的体内神经保护作用。
Neuroscience. 2009 Jan 23;158(2):514-23. doi: 10.1016/j.neuroscience.2008.10.041. Epub 2008 Oct 30.
10
NGX-4010, a high-concentration capsaicin patch, for the treatment of postherpetic neuralgia: a randomised, double-blind study.NGX-4010,一种高浓度辣椒素贴剂,用于治疗带状疱疹后神经痛:一项随机双盲研究。
Lancet Neurol. 2008 Dec;7(12):1106-12. doi: 10.1016/S1474-4422(08)70228-X. Epub 2008 Oct 30.

以神经保护为靶点,作为预防和治疗神经病理性疼痛的一种替代方法。

Targeting neuroprotection as an alternative approach to preventing and treating neuropathic pain.

机构信息

Trophos, Parc Scientifique de Luminy, Luminy Biotech Entreprises, 13288 Marseille, France.

出版信息

Neurotherapeutics. 2009 Oct;6(4):648-62. doi: 10.1016/j.nurt.2009.07.001.

DOI:10.1016/j.nurt.2009.07.001
PMID:19789070
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5084287/
Abstract

Neuropathic pain syndromes arise from dysfunction of the nerve itself, through traumatic or nontraumatic injury. Unlike acute pain syndromes, the pain is long-lasting and does not respond to common analgesic therapies. Drugs that disrupt nerve conduction and transmission or central sensitization, currently the only effective treatments, are only modestly effective for a portion of the patients suffering from neuropathic pain and come with the cost of serious adverse effects. Neurodegeneration, as a reaction to nerve trauma or chronic metabolic or chemical intoxication, appears to be an underlying cause of neuropathic pain. Identifying mechanisms of neurodegeneration and designing neuroprotective therapies is an ambitious goal toward treating or even preventing the development of these disabling disorders.

摘要

神经病理性疼痛综合征源于神经本身的功能障碍,可由创伤或非创伤性损伤引起。与急性疼痛综合征不同,其疼痛持续时间长,且对常用的镇痛疗法没有反应。目前唯一有效的治疗方法是破坏神经传导和传递或中枢敏化的药物,但对部分患有神经病理性疼痛的患者仅有一定的疗效,且存在严重不良反应的风险。神经退行性变是神经损伤或慢性代谢或化学中毒的反应,似乎是神经病理性疼痛的潜在原因。确定神经退行性变的机制并设计神经保护疗法是治疗甚至预防这些致残性疾病发展的一个宏伟目标。