Xing Yu, Xiao Yuan-Zhang, Zhao Min, Zhou Jiang-Jun, Zhao Kai, Xiao Chun-Lin
Department of Orthopaedics, Frist Affiliated Hospital of Gannan Medical University, Ganzhou, Jiangxi, China.
Gannan Medical University, 1 Harmony Avenue, Rongjiang New District, Ganzhou, Jiangxi Province, China.
Front Cell Neurosci. 2025 Jun 24;19:1590493. doi: 10.3389/fncel.2025.1590493. eCollection 2025.
Spinal cord ischemia/reperfusion injury (SCIRI) is a serious disease that leads to the loss of sensory and motor functions and is a common complication after spinal cord injury, spinal cord degeneration or thoracic and abdominal aortic surgery. At present, the spinal cord is mainly protected from ischemic injury through treatment strategies such as hypothermia, surgery and drug assistance, but these intervention measures cannot effectively improve these conditions. SCIRI is a complex process that leads to cell damage and death. Among them, oxidative stress is an important pathological event of ischemia/reperfusion injury. Oxidative stress can initiate multiple inflammatory and apoptotic pathways, triggering a series of destructive events such as inflammatory responses and cell death, further deteriorating the microenvironment at the injured site, and leading to neurological dysfunction. Based on the important role of oxidative stress in SCIRI, we believe that targeted inhibition of oxidative stress responses can effectively reduce secondary injuries caused by trauma, which has a certain positive effect on the rehabilitation and prognosis of patients with SCIRI. This review systematically expounds the spatiotemporal dynamic characteristics of oxidative stress during the SCIRI process and its molecular regulatory network, with a focus on analyzing the multivariate generation mechanism of ROS. To deeply explore the regulatory effects of ROS on pathological processes such as neuronal death, inflammatory response and blood-spinal barrier disruption under SCIRI conditions, as well as its interaction patterns with signaling pathways. In order to form a systematic treatment for SCIRI caused by oxidative stress and promote the recovery of neurological function after injury. This review is helpful for us to understand the effect of oxidative stress on SCIRI and provides a theoretical basis for the treatment of SCIRI based on oxidative stress.
脊髓缺血/再灌注损伤（SCIRI）是一种严重疾病，可导致感觉和运动功能丧失，是脊髓损伤、脊髓退变或胸腹主动脉手术后的常见并发症。目前，脊髓主要通过低温、手术和药物辅助等治疗策略来预防缺血性损伤，但这些干预措施并不能有效改善这些状况。SCIRI是一个导致细胞损伤和死亡的复杂过程。其中，氧化应激是缺血/再灌注损伤的重要病理事件。氧化应激可启动多种炎症和凋亡途径，引发一系列诸如炎症反应和细胞死亡等破坏性事件，进一步恶化损伤部位的微环境，并导致神经功能障碍。基于氧化应激在SCIRI中的重要作用，我们认为靶向抑制氧化应激反应可有效减少创伤引起的继发性损伤，这对SCIRI患者的康复和预后具有一定的积极作用。本综述系统阐述了SCIRI过程中氧化应激的时空动态特征及其分子调控网络，重点分析了活性氧（ROS）的多因素生成机制。深入探讨ROS在SCIRI条件下对神经元死亡、炎症反应和血脊髓屏障破坏等病理过程的调控作用，以及其与信号通路的相互作用模式。以期形成针对氧化应激所致SCIRI的系统治疗方法，促进损伤后神经功能的恢复。本综述有助于我们了解氧化应激对SCIRI的影响，并为基于氧化应激的SCIRI治疗提供理论依据。
