Journal
NEUROCHEMICAL RESEARCH
Volume 35, Issue 2, Pages 348-355Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-009-0061-2
Keywords
Edaravone; Traumatic brain injury; Neuroprotection; Apoptosis; Oxidative stress
Categories
Funding
- Grants-in-Aid for Scientific Research [21500803] Funding Source: KAKEN
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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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