Fang Yuepeng, Zhang Ce, Yang Zhijie, Zhao Xiangrui, Zhu Pengchong, Ning Bin
Jinan Central Hospital, Shandong University, No.105, Jiefang Road, Jinan, Shandong, 250013, China; Central Hospital Affiliated to Shandong First Medical University, No. 105, Jiefang Road, Jinan, Shandong, 250013, China.
Central Hospital Affiliated to Shandong First Medical University, No. 105, Jiefang Road, Jinan, Shandong, 250013, China.
Neuropharmacology. 2025 Nov 1;278:110591. doi: 10.1016/j.neuropharm.2025.110591. Epub 2025 Jul 21.
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.
本研究采用转录组测序和靶向代谢组学方法，深入探究脊髓损伤（SCI）后小鼠脊髓的分子变化。值得注意的是，在损伤的脊髓中观察到泛酸（PA）显著耗竭，且与小胶质细胞炎症和激活呈负相关。为进一步阐明这种关系，在SCI小鼠模型中进行了PA的实验干预。结果表明，给予PA可通过调节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，还营造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，接受PA治疗的SCI小鼠运动功能恢复得到改善。我们的研究结果不仅加深了对PA与SCI中神经炎症过程之间关系的理解，还突出了PA在促进神经元再生和功能恢复方面的治疗潜力。
