The effect of melatonin on spinal cord after ischemia in rats

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dc.authoridDilsiz, Nihat/0000-0002-0612-435X
dc.authoridaydemir, songul/0000-0002-7921-0662
dc.authorwosidDilsiz, Nihat/CAI-0100-2022
dc.authorwosidDilsiz, Nihat/AAF-3232-2021
dc.authorwosidaydemir, songul/AAA-4291-2021
dc.contributor.authorAydemir, S.
dc.contributor.authorDogan, D.
dc.contributor.authorKocak, A.
dc.contributor.authorDilsiz, N.
dc.date.accessioned2024-08-04T20:41:21Z
dc.date.available2024-08-04T20:41:21Z
dc.date.issued2016
dc.departmentİnönü Üniversitesien_US
dc.description.abstractStudy design: Experimental animal model to assess ischemic spinal cord injury (SCI) following occlusion of the thoracoabdominal aorta. Objectives: In the present study, we aimed to investigate the role of melatonin on SCI induced by ischemia and following reperfusion. Setting: Animal Research Laboratory, Inonu University, Malatya, Turkey. Methods: We evaluated oxidative damage and caspase-3 activity. In total, 32 adult Wistar albino rats were divided into four groups: Group 1, control (n=8); Group 2 (n=8), those subjected to ischemia/reperfusion (IR) by clamping the thoraco-abdominal aorta; Group 3 (n=8), melatonin (50 mg kg(-1)) treated; and Group 4 (n=8), melatonin (50 mg kg(-1)) followed by ischemia. All animals were kept alive for 48 h, and then spinal cord samples were removed. We assayed oxidative damage by measuring malondialdehyde (MDA), apoptosis by measuring activated caspase-3 (using immunoblots) and intrinsic antioxidative capacity by measuring reduced glutathione (GSH) levels in the spinal cord. Results: The results indicated a significant decrease in activity of caspase-3 in SCI animals after treatment with melatonin, as it significantly decreased the formation of MDA and decelerated the loss of GSH. Conclusion: This study suggested that melatonin could be an effective neuroprotective agent for treatment of SCI.en_US
dc.description.sponsorshipScientific and Research Project Unit of Inonu University, Turkey [BAP-2009004]en_US
dc.description.sponsorshipThis work was supported by a grant from The Scientific and Research Project Unit of Inonu University (BAP-2009004), Turkey.en_US
dc.identifier.doi10.1038/sc.2015.204
dc.identifier.endpage363en_US
dc.identifier.issn1362-4393
dc.identifier.issn1476-5624
dc.identifier.issue5en_US
dc.identifier.pmid26620879en_US
dc.identifier.scopus2-s2.0-84949032468en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage360en_US
dc.identifier.urihttps://doi.org/10.1038/sc.2015.204
dc.identifier.urihttps://hdl.handle.net/11616/97074
dc.identifier.volume54en_US
dc.identifier.wosWOS:000376192200005en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherNature Publishing Groupen_US
dc.relation.ispartofSpinal Corden_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectInjuryen_US
dc.subjectMechanismen_US
dc.subjectStressen_US
dc.subjectDeathen_US
dc.titleThe effect of melatonin on spinal cord after ischemia in ratsen_US
dc.typeArticleen_US

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