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

Molecular Medicine Reports
Jian GuoYongfu Li

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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Citations

Jan 24, 2018·Journal of Neurotrauma·Jean-Claude StamegnaFrançois S Roman
Aug 8, 2020·Frontiers in Cell and Developmental Biology·Lesang ShenJianmin Zhang

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Methods Mentioned

BETA
ELISA
protein assay

Software Mentioned

Image J
GraphPad Prism
GraphPad

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