Therapeutic Time Window for Edaravone Treatment of Traumatic Brain Injury in Mice

Traumatic brain injury (TBI) is a major cause of death and disability in young people. No effective therapy is available to ameliorate its damaging effects. Our aim was to investigate the optimal therapeutic time window of edaravone, a free radical scavenger which is currently used in Japan. We also...

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Main Authors:	Miyamoto, Kazuyuki, Ohtaki, Hirokazu, Dohi, Kenji, Tsumuraya, Tomomi, Song, Dandan, Kiriyama, Keisuke, Satoh, Kazue, Shimizu, Ai, Aruga, Tohru, Shioda, Seiji
Format:	Online
Language:	English
Published:	Hindawi Publishing Corporation 2013
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3654699/

id	pubmed-3654699
recordtype	oai_dc
spelling	pubmed-36546992013-05-24 Therapeutic Time Window for Edaravone Treatment of Traumatic Brain Injury in Mice Miyamoto, Kazuyuki Ohtaki, Hirokazu Dohi, Kenji Tsumuraya, Tomomi Song, Dandan Kiriyama, Keisuke Satoh, Kazue Shimizu, Ai Aruga, Tohru Shioda, Seiji Research Article Traumatic brain injury (TBI) is a major cause of death and disability in young people. No effective therapy is available to ameliorate its damaging effects. Our aim was to investigate the optimal therapeutic time window of edaravone, a free radical scavenger which is currently used in Japan. We also determined the temporal profile of reactive oxygen species (ROS) production, oxidative stress, and neuronal death. Male C57Bl/6 mice were subjected to a controlled cortical impact (CCI). Edaravone (3.0 mg/kg), or vehicle, was administered intravenously at 0, 3, or 6 hours following CCI. The production of superoxide radicals (O2 ∙−) as a marker of ROS, of nitrotyrosine (NT) as an indicator of oxidative stress, and neuronal death were measured for 24 hours following CCI. Superoxide radical production was clearly evident 3 hours after CCI, with oxidative stress and neuronal cell death becoming apparent after 6 hours. Edaravone administration after CCI resulted in a significant reduction in the injury volume and oxidative stress, particularly at the 3-hour time point. Moreover, the greatest decrease in O2 ∙− levels was observed when edaravone was administered 3 hours following CCI. These findings suggest that edaravone could prove clinically useful to ameliorate the devastating effects of TBI. Hindawi Publishing Corporation 2013 2013-04-10 /pmc/articles/PMC3654699/ /pubmed/23710445 http://dx.doi.org/10.1155/2013/379206 Text en Copyright © 2013 Kazuyuki Miyamoto et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Miyamoto, Kazuyuki Ohtaki, Hirokazu Dohi, Kenji Tsumuraya, Tomomi Song, Dandan Kiriyama, Keisuke Satoh, Kazue Shimizu, Ai Aruga, Tohru Shioda, Seiji
spellingShingle	Miyamoto, Kazuyuki Ohtaki, Hirokazu Dohi, Kenji Tsumuraya, Tomomi Song, Dandan Kiriyama, Keisuke Satoh, Kazue Shimizu, Ai Aruga, Tohru Shioda, Seiji Therapeutic Time Window for Edaravone Treatment of Traumatic Brain Injury in Mice
author_facet	Miyamoto, Kazuyuki Ohtaki, Hirokazu Dohi, Kenji Tsumuraya, Tomomi Song, Dandan Kiriyama, Keisuke Satoh, Kazue Shimizu, Ai Aruga, Tohru Shioda, Seiji
author_sort	Miyamoto, Kazuyuki
title	Therapeutic Time Window for Edaravone Treatment of Traumatic Brain Injury in Mice
title_short	Therapeutic Time Window for Edaravone Treatment of Traumatic Brain Injury in Mice
title_full	Therapeutic Time Window for Edaravone Treatment of Traumatic Brain Injury in Mice
title_fullStr	Therapeutic Time Window for Edaravone Treatment of Traumatic Brain Injury in Mice
title_full_unstemmed	Therapeutic Time Window for Edaravone Treatment of Traumatic Brain Injury in Mice
title_sort	therapeutic time window for edaravone treatment of traumatic brain injury in mice
description	Traumatic brain injury (TBI) is a major cause of death and disability in young people. No effective therapy is available to ameliorate its damaging effects. Our aim was to investigate the optimal therapeutic time window of edaravone, a free radical scavenger which is currently used in Japan. We also determined the temporal profile of reactive oxygen species (ROS) production, oxidative stress, and neuronal death. Male C57Bl/6 mice were subjected to a controlled cortical impact (CCI). Edaravone (3.0 mg/kg), or vehicle, was administered intravenously at 0, 3, or 6 hours following CCI. The production of superoxide radicals (O2 ∙−) as a marker of ROS, of nitrotyrosine (NT) as an indicator of oxidative stress, and neuronal death were measured for 24 hours following CCI. Superoxide radical production was clearly evident 3 hours after CCI, with oxidative stress and neuronal cell death becoming apparent after 6 hours. Edaravone administration after CCI resulted in a significant reduction in the injury volume and oxidative stress, particularly at the 3-hour time point. Moreover, the greatest decrease in O2 ∙− levels was observed when edaravone was administered 3 hours following CCI. These findings suggest that edaravone could prove clinically useful to ameliorate the devastating effects of TBI.
publisher	Hindawi Publishing Corporation
publishDate	2013
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3654699/
_version_	1611977971220873216

Therapeutic Time Window for Edaravone Treatment of Traumatic Brain Injury in Mice

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