Pantothenic acid-mediated inhibition of microglial inflammation via the JAK2/STAT3 pathway enhances motor function recovery after Spinal cord injury

IF 4.6 2区医学 Q1 NEUROSCIENCES

Neuropharmacology Pub Date : 2025-07-21 DOI:10.1016/j.neuropharm.2025.110591

Yuepeng Fang , Ce Zhang , Zhijie Yang , Xiangrui Zhao , yongcheng Yin , zhengxin Jin , Pengchong Zhu , Bin Ning

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引用次数: 0

Abstract

This study employed transcriptome sequencing and targeted metabolomics to delve into the molecular alterations in mouse spinal cords following spinal cord injury (SCI). Notably, a significant depletion of pantothenic acid (PA) was observed in the injured spinal cord, exhibiting an inverse correlation with microglial inflammation and activation. To further elucidate this relationship, experimental interventions using PA were conducted in SCI mouse models. The results demonstrated that PA administration effectively inhibited microglial inflammation via modulation of the JAK2/STAT3 signaling pathway. This inhibition not only mitigated the neuroinflammatory milieu but also fostered an environment conducive to axonal growth and neuronal regeneration. Consequently, SCI mice treated with PA exhibited improved motor function recovery compared to untreated controls. Our findings not only deepen the understanding of the relationship between PA and neuroinflammatory processes in SCI but also highlight the therapeutic potential of PA in promoting neuronal regeneration and functional recovery.

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泛酸通过JAK2/STAT3途径介导的小胶质细胞炎症抑制促进脊髓损伤后运动功能的恢复。

本研究采用转录组测序和靶向代谢组学研究小鼠脊髓损伤（SCI）后的分子变化。值得注意的是，在损伤的脊髓中观察到明显的泛酸（PA）消耗，与小胶质细胞炎症和激活呈负相关。为了进一步阐明这种关系，我们在脊髓损伤小鼠模型中使用PA进行了实验干预。结果表明，PA通过调节JAK2/STAT3信号通路有效抑制小胶质细胞炎症。这种抑制不仅减轻了神经炎症环境，而且还培养了有利于轴突生长和神经元再生的环境。因此，与未治疗的对照组相比，用PA治疗的脊髓损伤小鼠表现出更好的运动功能恢复。我们的研究结果不仅加深了对脊髓损伤中PA与神经炎症过程之间关系的理解，而且强调了PA在促进神经元再生和功能恢复方面的治疗潜力。

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

Neuropharmacology 医学-神经科学

CiteScore

10.00

自引率

4.30%

发文量

288

审稿时长

45 days

期刊介绍： Neuropharmacology publishes high quality, original research and review articles within the discipline of neuroscience, especially articles with a neuropharmacological component. However, papers within any area of neuroscience will be considered. The journal does not usually accept clinical research, although preclinical neuropharmacological studies in humans may be considered. The journal only considers submissions in which the chemical structures and compositions of experimental agents are readily available in the literature or disclosed by the authors in the submitted manuscript. Only in exceptional circumstances will natural products be considered, and then only if the preparation is well defined by scientific means. Neuropharmacology publishes articles of any length (original research and reviews).