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电针对慢性炎症大鼠疼痛和疼痛相关焦虑的抑制作用是通过增加 ACC 中 NPS/NPSR 系统的表达来实现的。

Electroacupuncture suppresses the pain and pain-related anxiety of chronic inflammation in rats by increasing the expression of the NPS/NPSR system in the ACC.

机构信息

Department of Neurobiology and Acupuncture Research, the Third Clinical Medical College, Zhejiang Chinese Medical University, Key Laboratory of Acupuncture and Neurology of Zhejiang Province, Hangzhou 310053, China.

Department of Neurobiology and Acupuncture Research, the Third Clinical Medical College, Zhejiang Chinese Medical University, Key Laboratory of Acupuncture and Neurology of Zhejiang Province, Hangzhou 310053, China.

出版信息

Brain Res. 2020 Apr 15;1733:146719. doi: 10.1016/j.brainres.2020.146719. Epub 2020 Feb 7.

DOI:10.1016/j.brainres.2020.146719
PMID:32044336
Abstract

BACKGROUND

The neuropeptide S/Neuropeptide S receptor (NPS/NPSR) system is involved in the regulation of anxiety in rodents. Chronic inflammation can induce anxiety. Our lab has observed that electroacupuncture (EA) has a beneficial effect on chronic inflammatory pain and pain-related anxiety; however, the mechanism should be further clarified. In the present study, we used an inflammatory pain model to investigate the role of the NPS/NPSR system in the anterior cingulate cortex (ACC) in the analgesic and antianxiety effects of EA.

RESULTS

In an inflammatory pain model, the paw withdrawal thresholds (PWTs) were decreased, pain-related anxiety-like behaviors were induced, and the ipsilateral protein expression of NPS and NPSR was decreased in the ACC. EA stimulation increased the PWTs, reduced pain-related anxiety-like behavior, and enhanced the ipsilateral protein expression of NPS and NPSR in the ACC. NPS microinjection increased the PWTs and decreased pain-related anxiety-like behaviors. Furthermore, an NPSR inhibitor combined with EA reversed the effect of EA on the PWTs and pain-related anxiety-like behaviors.

CONCLUSIONS

Our results suggest that EA suppresses pain and pain-related anxiety-like behavior of chronic inflammation in rats by increasing the expression of the NPS/NPSR system in the ACC.

摘要

背景

神经肽 S/神经肽 S 受体(NPS/NPSR)系统参与调节啮齿动物的焦虑。慢性炎症可诱发焦虑。我们实验室观察到电针(EA)对慢性炎症性疼痛和与疼痛相关的焦虑具有有益作用;然而,其机制尚需进一步阐明。在本研究中,我们使用炎症性疼痛模型,探讨 NPS/NPSR 系统在 ACC 中在 EA 的镇痛和抗焦虑作用中的作用。

结果

在炎症性疼痛模型中,足底缩足阈值(PWT)降低,诱导出与疼痛相关的焦虑样行为,并且 ACC 中的 NPS 和 NPSR 蛋白表达减少。EA 刺激增加了 PWT,减少了与疼痛相关的焦虑样行为,并增强了 ACC 中 NPS 和 NPSR 的同侧蛋白表达。NPS 微注射增加了 PWT 并减少了与疼痛相关的焦虑样行为。此外,NPSR 抑制剂与 EA 联合使用逆转了 EA 对 PWT 和与疼痛相关的焦虑样行为的影响。

结论

我们的结果表明,EA 通过增加 ACC 中 NPS/NPSR 系统的表达来抑制大鼠慢性炎症引起的疼痛和与疼痛相关的焦虑样行为。

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