MCTR1 alleviates remifentanil-induced hyperalgesia by regulating mitochondrial fission protein DRP1 in rats.

IF 1.7 4区医学 Q4 NEUROSCIENCES

Neuroreport Pub Date : 2025-09-03 Epub Date: 2025-07-17 DOI:10.1097/WNR.0000000000002198

Lijun Gu, Linyao Chen, Yanan Wang, Linglin Gao, Jianwen Ye, Zixuan Xu, Zijun Zhou, Jiehao Sun

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引用次数: 0

Abstract

Objective: This study aimed to investigate whether Maresin conjugates in tissue regeneration-1 (MCTR1) can alleviate remifentanil-induced hyperalgesia (RIH) by modulating the mitochondrial fission protein dynamin-related protein 1 (DRP1).

Methods: Pain behavioral tests were conducted 24 h before remifentanil infusion and at 4, 8, and 24 h postinfusion. The expression of DRP1 and NR2B was assessed by Western Blot (WB). Additionally, intrathecal injections of MCTR1 were administered to evaluate the effects on RIH development and progression. Behavioral tests were conducted, meanwhile, the levels of DRP1, NR2B in the spinal cord, superoxide, including malondialdehyde (MDA), glutathione, and reactive oxygen species (ROS) in the spinal dorsal horn were measured. Mitochondrial numbers were counted via transmission electron-microscopy.

Results: After remifentanil administration, rats exhibited mechanical allodynia and thermal hyperalgesia, along with an increase in spinal levels of DRP1 and NR2B. However, MCTR1-treated rats showed alleviation of remifentanil-induced mechanical and thermal hyperalgesia, accompanied by reduced NR2B expression. Notably, MCTR1 treatment also led to decreased DRP1 expression and mitochondrial fission, as well as reduced MDA content and ROS production.

Conclusion: MCTR1 exerts a preventive effect on RIH by modulating NR2B activity through the DRP1-mitochondrial-ROS pathway.

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MCTR1通过调节线粒体裂变蛋白DRP1减轻瑞芬太尼诱导的大鼠痛觉过敏。

目的：本研究旨在探讨Maresin偶联物组织再生-1 （MCTR1）是否通过调节线粒体裂变蛋白动力蛋白相关蛋白1 （DRP1）减轻瑞芬太尼诱导的痛觉过敏（RIH）。方法：在瑞芬太尼输注前24 h和输注后4、8、24 h分别进行疼痛行为测试。Western Blot （WB）检测DRP1和NR2B的表达。此外，鞘内注射MCTR1以评估对RIH发生和进展的影响。进行行为学实验，同时测定脊髓DRP1、NR2B、脊髓背角超氧化物包括丙二醛（MDA）、谷胱甘肽、活性氧（ROS）水平。透射电镜观察线粒体数量。结果：瑞芬太尼给药后，大鼠表现出机械异常性痛和热痛觉过敏，脊髓DRP1和NR2B水平升高。然而，mctr1处理的大鼠显示瑞芬太尼引起的机械和热痛觉过敏减轻，并伴有NR2B表达降低。值得注意的是，MCTR1处理还导致DRP1表达和线粒体分裂降低，MDA含量和ROS生成降低。结论：MCTR1通过drp1 -线粒体- ros通路调节NR2B活性，对RIH具有预防作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Neuroreport 医学-神经科学

CiteScore

3.20

自引率

0.00%

发文量

150

审稿时长

1 months

期刊介绍： NeuroReport is a channel for rapid communication of new findings in neuroscience. It is a forum for the publication of short but complete reports of important studies that require very fast publication. Papers are accepted on the basis of the novelty of their finding, on their significance for neuroscience and on a clear need for rapid publication. Preliminary communications are not suitable for the Journal. Submitted articles undergo a preliminary review by the editor. Some articles may be returned to authors without further consideration. Those being considered for publication will undergo further assessment and peer-review by the editors and those invited to do so from a reviewer pool. The core interest of the Journal is on studies that cast light on how the brain (and the whole of the nervous system) works. We aim to give authors a decision on their submission within 2-5 weeks, and all accepted articles appear in the next issue to press.