Brain and Behavior, 2023 · DOI: 10.1002/brb3.2870 · Published: January 1, 2023
Traumatic spinal cord injury (SCI) is a common and devastating central nervous disease. Treatment measures based on oxidative stress of spinal motor neurons during SCI are expected to help restore biological functions of neurons under injury conditions. However, to date, there are no systematic reports regarding oxidative stress on spinal motor neuron injury. The study exposed VSC4.1 motor neurons to hydrogen peroxide (H2O2) and evaluated the effects on cell viability, morphology, cycling, and apoptosis, with an emphasis on the changes to the cytoskeleton and the effect of N-acetyl-L-cysteine (NAC) on these changes. Then, the study investigated the effects of NAC on these cytoskeletal changes in vitro and in vivo. The study found that H2O2 caused severe damage to the normal cytoskeleton, leading to a reduction in neurite length and number, rearrangement of the actin cytoskeleton, and disorder of the microtubules and neurofilaments in VSC4.1. NAC attenuated the oxidative damage of spinal motor neurons in vitro and in vivo, promoting the recovery of hindlimb motor ability in mice with SCI at the early stage of injury.
Targeting oxidative stress in SCI treatment is a promising strategy.
Oxidative stress-induced cytoskeleton repair has potential to promote functional recovery after central nervous system injury.
Further studies are needed to explore the effect and mechanism of oxidative stress on spinal motor neuron injury after SCI.