Edaravone attenuates traumatic brain injury through anti-inflammatory and anti-oxidative modulation

Traumatic brain injury (TBI) is among the leading causes of irreversible neurological damage and death worldwide. The aim of the present study was to investigate whether edaravone (EDA) had a neuroprotective effect on TBI as well as to identify the potential mechanism. Results demonstrated that EDA...

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Bibliographic Details
Published in:Experimental and therapeutic medicine 2019-07, Vol.18 (1), p.467-474
Main Authors: Zhang, Man, Teng, Chen-Huai, Wu, Fang-Fang, Ge, Li-Yun, Xiao, Jian, Zhang, Hong-Yu, Chen, Da-Qing
Format: Article
Language:English
Subjects:
Anti-inflammatory agents
Antioxidants (Nutrients)
Apoptosis
Biotechnology industries
Brain injuries
Edaravone
Free radicals
Hydrogen peroxide
Immunoglobulins
Inflammation
Interleukins
Ischemia
Medical research
Necrosis
Oxidative stress
Peroxidase
Peroxides
Quinones
Studies
Superoxides
Traumatic brain injury
Tumor necrosis factor
Tumor necrosis factor-TNF
Tumors
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Summary:Traumatic brain injury (TBI) is among the leading causes of irreversible neurological damage and death worldwide. The aim of the present study was to investigate whether edaravone (EDA) had a neuroprotective effect on TBI as well as to identify the potential mechanism. Results demonstrated that EDA suppressed inflammatory and oxidative responses in mice following TBI. This was evidenced by a reduction in glutathione peroxidase, interleukin 6, tumor necrosis factor-α and hydrogen peroxide levels, in addition to an increase in hemeoxygenase-1, quinone oxidoreductase 1 and superoxide dismutase levels, thereby mitigating neurofunctional deficits, cell apoptosis and structural damage. EDA prevented the transfer of NF-κB protein from the cytoplasm to the nucleus, whilst promoting the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) protein in mice following TBI. These results indicated that EDA exerted neuroprotective effects, including impeding neurofunctional deficits, cell apoptosis and structural damage, in mice with TBI, potentially via suppression of NF-κB-mediated inflammatory activation and promotion of the Nrf2 antioxidant pathway.
ISSN:1792-0981
1792-1015
DOI:10.3892/etm.2019.7632