Protective Effects of Edaravone on Experimental Spinal Cord Injury in Rats

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dc.authoridZileli, Mehmet/0000-0002-0448-3121
dc.contributor.authorOzgiray, Erkin
dc.contributor.authorSerarslan, Yurdal
dc.contributor.authorOzturk, Oktay Hasan
dc.contributor.authorAltas, Murat
dc.contributor.authorAras, Mustafa
dc.contributor.authorSogut, Sadik
dc.contributor.authorYurtseven, Taskin
dc.date.accessioned2024-09-18T19:54:38Z
dc.date.available2024-09-18T19:54:38Z
dc.date.issued2011
dc.departmentHatay Mustafa Kemal Üniversitesien_US
dc.description.abstractBackground: Spinal cord injury (SCI) is a leading cause of morbidity and mortality among youth and adults. Secondary injury mechanisms within the spinal cord (SC) are well known to cause deterioration after an acute impact. Free radical scavengers are among the most studied agents in animal models of SCI. Edaravone is a scavenger of hydroxyl radicals. Methods: We aimed to measure and compare the effects of both methylprednisolone and edaravone on tissue and on serum concentrations of nitric oxide (NO), malondialdehyde (MDA) levels, superoxide dismutase (SOD) activity, glutathione peroxidase (GSH-Px) activity, and tissue total antioxidant capacity (TAC) in rats with SCI. SCI was induced in four groups of Wistar albino rats by a weight-drop method. The neurological function of the rats was periodically tested. At the end of the experiment, blood samples were collected, and SC tissue samples were harvested for biochemical evaluation. Results: The tissue level of NO was decreased in the edaravone-treated group compared with the no-treatment group (p < 0.05). The tissue levels of SOD and GSH-Px were higher in the edaravone-treated group than in the no-treatment group (p < 0.05). The serum levels of NO were lower in the edaravone-treated and methylprednisolone-treated groups than in the no-treatment group (p < 0.05). The serum levels of SOD in the edaravone-treated group did not differ from those of any other group. The serum levels of MDA in the edaravone-treated and no-treatment groups were higher than in the two other groups (p < 0.05). Tissue levels of MDA in the edaravone-treated group were lower than in the no-treatment group (p < 0.05). Tissue levels of TAC in the edaravone-treated group were higher than in the no-treatment and methylprednisolone-treated groups (p < 0.05). The neurological outcome scores of the animals in treatment groups did not depict any statistically significant improvement in motor functions. However, edaravone seemed to prevent further worsening of the immediate post-SCI neurological status. Conclusion: Our biochemical analyses indicate that edaravone is capable of blunting the increased oxidative stress that follows SCI. We show, for the first time, that edaravone enhances the TAC in SC tissue. This beneficial effect of edaravone on antioxidant status may act to minimize the secondary neurological damage that occurs during the acute phase after SCI. Copyright (C) 2012 S. Karger AG, Baselen_US
dc.identifier.doi10.1159/000335400
dc.identifier.endpage260en_US
dc.identifier.issn1016-2291
dc.identifier.issn1423-0305
dc.identifier.issue4en_US
dc.identifier.pmid22310070en_US
dc.identifier.scopus2-s2.0-84861096511en_US
dc.identifier.scopusqualityQ3en_US
dc.identifier.startpage254en_US
dc.identifier.urihttps://doi.org/10.1159/000335400
dc.identifier.urihttps://hdl.handle.net/20.500.12483/7833
dc.identifier.volume47en_US
dc.identifier.wosWOS:000305637300003en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherKargeren_US
dc.relation.ispartofPediatric Neurosurgeryen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectAntioxidanten_US
dc.subjectRaten_US
dc.subjectSpinal cord injuryen_US
dc.subjectEdaravoneen_US
dc.subjectTotal antioxidant capacityen_US
dc.titleProtective Effects of Edaravone on Experimental Spinal Cord Injury in Ratsen_US
dc.typeArticleen_US

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