Wei Yiling, Xu Xianlin, Wu Pan, Chen Xiang, Mo Qingmei, Zhuo Ming
Medical School, Guizhou University, Guiyang 550000, China.
Department of Biochemistry, School of Preclinical Medicine, Zunyi Medical University, Zunyi 563100, China.
Curr Issues Mol Biol. 2025 Jun 24;47(7):482. doi: 10.3390/cimb47070482.
Nerve injury caused by chemotherapy drugs is a common side effect. How to reduce this kind of nerve injury and promote neuron recovery is of great significance. In this study, we found that tumor necrosis factor-α (TNF-α) promoted the recovery of dorsal root ganglion (DRG) neuron from cisplatin-induced injury. On DRG neurons cultured in vitro, we found that TNF-α promoted neurite regeneration after cisplatin injury. In addition, TNF-α accelerated the removal of DNA damage and promoted the regeneration of mitochondria on DRG neurons. Study of the mechanism showed that this effect of TNF-α was independent from the NGF signaling pathway and occurred mostly through the activation of TNFR2 receptors, together with nucleus translocation of p65 and upregulation of NF-κB expression. This study provides a new theoretical basis and therapeutic strategy for the treatment of nerve injury caused by chemotherapy drugs.
化疗药物引起的神经损伤是一种常见的副作用。如何减少这种神经损伤并促进神经元恢复具有重要意义。在本研究中，我们发现肿瘤坏死因子-α（TNF-α）促进背根神经节（DRG）神经元从顺铂诱导的损伤中恢复。在体外培养的DRG神经元上，我们发现TNF-α促进顺铂损伤后的神经突再生。此外，TNF-α加速了DNA损伤的清除，并促进了DRG神经元上的线粒体再生。机制研究表明，TNF-α的这种作用独立于NGF信号通路，主要通过激活TNFR2受体，伴随p65核转位和NF-κB表达上调而发生。本研究为化疗药物所致神经损伤的治疗提供了新的理论依据和治疗策略。
