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Edaravone protects against apoptotic neuronal cell death and improves cerebral function after traumatic brain injury in rats.

Authors
  • Itoh, Tatsuki
  • Satou, Takao
  • Nishida, Shozo
  • Tsubaki, Masahiro
  • Imano, Motohiro
  • Hashimoto, Shigeo
  • Ito, Hiroyuki
Type
Published Article
Journal
Neurochemical Research
Publisher
Springer-Verlag
Publication Date
Feb 01, 2010
Volume
35
Issue
2
Pages
348–355
Identifiers
DOI: 10.1007/s11064-009-0061-2
PMID: 19768539
Source
Medline
License
Unknown

Abstract

Edaravone is a novel free radical scavenger used clinically in patients with acute cerebral infarction; however, it has not been assessed in traumatic brain injury (TBI). We investigated the effects of edaravone on cerebral function and morphology following TBI. Rats received TBI with a pneumatic controlled injury device. Edaravone (3 mg/kg) or physiological saline was administered intravenously following TBI. Numbers of 8-OHdG-, 4-HNE-, and ssDNA-positive cells around the damaged area after TBI were significantly decreased in the edaravone group compared with the saline group (P < 0.01). There was a significant increase in neuronal cell number and improvement in cerebral dysfunction after TBI in the edaravone group compared with the saline group (P < 0.01). Edaravone administration following TBI inhibited free radical-induced neuronal degeneration and apoptotic cell death around the damaged area. In summary, edaravone treatment improved cerebral dysfunction following TBI, suggesting its potential as an effective clinical therapy.

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