PNAS：慢性疼痛患者的福音

2015-07-13 佚名生物谷

近日，来自加州大学戴维斯分校的研究人员发现了神经疼痛的重要机制。他们发现，被称为内质网应激的生物过程，是引起神经疼痛的重要原因。这项发现可能造福于成千上万的慢性疼痛的患者，例如由创伤，糖尿病，带状疱疹，多发性硬化症或导致神经损伤的其他疾病引起的慢性疼痛。相关研究成果于近日发表在PNAS杂志上。最近，有研究发现, 非通道、非神经递质的疼痛治疗靶点是可溶性环氧化物水解酶(sEH)。这种酶可以降解自然镇

近日，来自加州大学戴维斯分校的研究人员发现了神经疼痛的重要机制。他们发现，被称为内质网应激的生物过程，是引起神经疼痛的重要原因。这项发现可能造福于成千上万的慢性疼痛的患者，例如由创伤，糖尿病，带状疱疹，多发性硬化症或导致神经损伤的其他疾病引起的慢性疼痛。相关研究成果于近日发表在PNAS杂志上。

最近，有研究发现, 非通道、非神经递质的疼痛治疗靶点是可溶性环氧化物水解酶(sEH)。这种酶可以降解自然镇痛脂类介质，环氧脂肪酸(EpFAs)。因此，抑制这种酶，可以稳定这些生物活性介质。在本文的研究中，研究人员们发现了EpFAs在糖尿病引起的神经痛中的效应，并确定出一种先前未知的疼痛机制，即被称为内质网应激的生物过程。首先，研究人员们利用大鼠的一型糖尿病模型，量化了外周神经系统激活的内质网应激。接着，他们发现，用一种化学分子伴侣可以缓解疼痛和内质网应激。而且，EpFAs是内质网应激通路上游的调制器。由化学因素引起的疼痛，均可以被化学分子伴侣或者sEH抑制剂所缓解。这种由疼痛诱导剂引起的快速疼痛，以及用阻断剂即可快速缓解的疼痛，和在糖尿病外周神经系统，自然发生的内质网应激，均可以证明，内质网应激通路在调解疼痛系统活性方面的重要作用。

这项研究发现阐明了一种神经痛的新机制。根据这项新机制，研究人员将研发出新的阻断内质网应激的药物，进行临床试验。同时，研究人员还将开展基础研究，辨别引起神经痛的不同机制，及新型药物对这些不用种类的神经痛的效果。

原始出处：

Bora Inceoglua,1, Ahmed Bettaiebb,1, Carlos A. Trindade da Silvaa, Kin Sing Stephen Leea, Fawaz G. Hajb,c,2, and Bruce D. Hammocka,2.Endoplasmic reticulum stress in the peripheral nervous system is a significant driver of neuropathic pain.PNAS.July 6, 2015.doi: 10.1073/pnas.1510137112

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2023-03-23 ms3000001190147103 来自山东省

很好的文章

58 0
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2017-06-20 戒馋，懒，贪

从研究结果到临床应用，还有好久的路啊

68 0
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2016-09-15 1e10c84am36(暂无匿称)

文章不错，值得拜读

51 0
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2016-03-30 忠诚向上

好好学习一下

70 0
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2016-03-30 忠诚向上

好好学习一下

99 0
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2016-03-30 忠诚向上

好好学习一下

112 0
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2016-03-30 忠诚向上

好好学习一下

94 0
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2016-03-30 忠诚向上

好好学习一下

75 0
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2016-03-30 忠诚向上

好好学习一下

67 0
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2016-03-30 忠诚向上

好好学习一下

97 0

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