N-acetylcysteine treatment following spinal cord trauma reduces neural tissue damage and improves locomotor function in mice

Guo,Jian; Li,Yiqiao; Chen,Zhong; He,Zhennian; Zhang,Bin; Li,Yonghuan; Hu,Jianghua; Han,Mingyuan; Xu,Yuanlin; Li,Yongfu

doi:10.3892/mmr.2015.3390

N-acetylcysteine treatment following spinal cord trauma reduces neural tissue damage and improves locomotor function in mice

Authors:
- Jian Guo
- Yiqiao Li
- Zhong Chen
- Zhennian He
- Bin Zhang
- Yonghuan Li
- Jianghua Hu
- Mingyuan Han
- Yuanlin Xu
- Yongfu Li
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Affiliations: Department of Orthopaedic Surgery, Ningbo Beilun People Hospital, Ningbo, Zhejiang 315800, P.R. China, Central Laboratory, Ningbo Beilun People Hospital, Ningbo, Zhejiang 315800, P.R. China
Published online on: February 26, 2015 https://doi.org/10.3892/mmr.2015.3390
Pages: 37-44
Copyright: © Guo et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0].

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Abstract

Following spinal cord trauma, mitochondrial dysfunction associated with increased oxidative stress is a critical event leading to leukocyte inflammatory responses, neuronal cell death and demyelination, contributing to permanent locomotor and neurological disability. The present study demonstrated that the mitochondrial enhancer N‑acetylcysteine (NAC) may restore redox balance via enhancement of mitochondrial respiratory activity following traumatic spinal cord injury (SCI). In addition, NAC ameliorates oxidative stress‑induced neuronal loss, demyelination, leukocyte infiltration and inflammatory mediator expression and improves long‑term locomotor function. Furthermore, neuronal survival and neurological recovery are significantly correlated with increased mitochondrial bioenergetics in SCI following treatment with NAC. Therefore, NAC may represent a potential therapeutic agent for preserving mitochondrial dynamics and integrity following traumatic SCI.

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