N-acetylcysteine treatment following spinal cord trauma reduces neural tissue damage and improves locomotor function in mice.
Mol Med Rep
; 12(1): 37-44, 2015 Jul.
Article
in En
| MEDLINE
| ID: mdl-25738883
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.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Acetylcysteine
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Spinal Cord Injuries
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Neuroprotective Agents
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Motor Activity
Limits:
Animals
/
Humans
Language:
En
Journal:
Mol Med Rep
Year:
2015
Document type:
Article