表达:PDCD4抑制通过调节脊髓自噬和神经炎症减轻神经性疼痛。

IF 2.8 3区 医学 Q2 NEUROSCIENCES
Molecular Pain Pub Date : 2025-01-01 Epub Date: 2025-03-28 DOI:10.1177/17448069251333928
Ting Zhang, Le Qi, Kai Sun, Xiang Huan, Hao Zhang, Liwei Wang
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引用次数: 0

摘要

神经性疼痛仍然是一个临床挑战。脊髓的炎症反应和自噬是神经性疼痛发生和维持的重要机制。PDCD4是调节炎症和自噬的重要分子。然而,PDCD4在疼痛调节中的调节作用尚不清楚。本研究发现CCI小鼠脊髓中PDCD4表达升高。鞘内注射腺相关病毒抑制PDCD4减轻了CCI小鼠的神经性疼痛超敏反应,增强了自噬,抑制了MAPKs的激活以及炎症因子的表达。鞘内注射自噬抑制剂3-MA可逆转PDCD4抑制引起的疼痛缓解和自噬的改变。我们的研究结果表明,脊髓抑制PDCD4可减轻神经性疼痛小鼠的疼痛致敏,PDCD4可能成为神经性疼痛治疗的治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
PDCD4 inhibition alleviates neuropathic pain by regulating spinal autophagy and neuroinflammation.

Neuropathic pain is still a clinical challenge. Inflammatory responses and autophagy in the spinal cord are important mechanisms for the occurrence and maintain of neuropathic pain. PDCD4 is an important molecule that regulates inflammation and autophagy. However, the regulatory role of PDCD4 is unknown in pain modulation. In this study we found that the expression of PDCD4 in the spinal cord of CCI mice was increased. Inhibition of PDCD4 by intrathecal injection of adeno-associated virus alleviated neuropathic pain hypersensitivity and enhanced autophagy in CCI mice, and inhibited the activation of MAPKs, as well as the expression of inflammatory factors. Intrathecal injection of autophagy inhibitor 3-MA reversed PDCD4 inhibition induced pain relief and change of autophagy. Our results indicate that spinal cord inhibition of PDCD4 alleviates pain sensitization in neuropathic pain mice through MAPKs and autophagy, and PDCD4 may be developed into a therapeutic target of neuropathic pain treatment.

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来源期刊
Molecular Pain
Molecular Pain 医学-神经科学
CiteScore
5.60
自引率
3.00%
发文量
56
审稿时长
6-12 weeks
期刊介绍: Molecular Pain is a peer-reviewed, open access journal that considers manuscripts in pain research at the cellular, subcellular and molecular levels. Molecular Pain provides a forum for molecular pain scientists to communicate their research findings in a targeted manner to others in this important and growing field.
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