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

Abstract:

: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.

journal_name

Exp Ther Med

authors

Zhang M,Teng CH,Wu FF,Ge LY,Xiao J,Zhang HY,Chen DQ

doi

10.3892/etm.2019.7632

subject

Has Abstract

pub_date

2019-07-01 00:00:00

pages

467-474

issue

1

eissn

1792-0981

issn

1792-1015

pii

ETM-0-0-7632

journal_volume

18

pub_type

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