The effects of prophylactic zinc and melatonin application on experimental spinal cord ischemia-reperfusion injury in rabbits: experimental study

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dc.contributor.authorKalkan, E.
dc.contributor.authorÇiçek, O.
dc.contributor.authorÜnlü, Ali
dc.contributor.authorAbuşoğlu, Sedat
dc.contributor.authorKalkan, S. S.
dc.contributor.authorAvunduk, M. C.
dc.contributor.authorBaysefer, A.
dc.date.accessioned2020-03-26T17:18:30Z
dc.date.available2020-03-26T17:18:30Z
dc.date.issued2007
dc.departmentSelçuk Üniversitesien_US
dc.description.abstractStudy design: Experimental study. Objectives: To determine the neuroprotective effects of zinc and melatonin on spinal cord ischemia-reperfusion (I/R) injuries of rabbits. Setting: The Experimental Research Centre of Selcuk University, Konya, Turkey. Methods: Twenty-four male rabbits underwent spinal cord ischemia by clamping the thoraco-abdominal aorta for 20 min. Twenty-minutes before the aortic clamping, animals received zinc, melatonin or a combination of both. Neurological examination of the animals was performed three times during reperfusion period. The animals were killed 24 h after reperfusion. Spinal cord samples were taken for biochemical and histopathological evaluation. Results: Pre-treated animals with zinc, melatonin or combination displayed better neurological outcomes than the I/R group (P < 0.05). Zinc, melatonin and combined treatment prevented spinal cord injury by reducing apoptosis rate (P < 0.05) and preserving intact ganglion cell numbers (P < 0.05). Zinc pre-treatment protected spinal cord by preventing malondialdehyde (MDA) formation (P = 0.002), increasing glutathione peroxidase (GPx) activity(P = 0.002) and decreasing xanthine oxidase enzyme activity (P = 0.026) at molecular level. Melatonin treatment also resulted with MDA formation (P = 0.002), increased GPx activity (P = 0.002) and decreased xanthine oxidase activity(P = 0.026). Conclusion: The results of the study showed that prophylactic zinc and melatonin use in spinal cord I/R not only suppressed lipid peroxidation by activating antioxidant systems but also had significant neuroprotective effects by specifically improving the neurological and histopathological situation.en_US
dc.identifier.doi10.1038/sj.sc.3102035en_US
dc.identifier.endpage730en_US
dc.identifier.issn1362-4393en_US
dc.identifier.issue11en_US
dc.identifier.pmid17297496en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage722en_US
dc.identifier.urihttps://dx.doi.org/10.1038/sj.sc.3102035
dc.identifier.urihttps://hdl.handle.net/20.500.12395/21678
dc.identifier.volume45en_US
dc.identifier.wosWOS:000250658500003en_US
dc.identifier.wosqualityQ3en_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.selcuk20240510_oaigen_US
dc.subjectischemiaen_US
dc.subjectreperfusionen_US
dc.subjectzincen_US
dc.subjectmelatoninen_US
dc.subjectoxidative damageen_US
dc.subjectrabbiten_US
dc.titleThe effects of prophylactic zinc and melatonin application on experimental spinal cord ischemia-reperfusion injury in rabbits: experimental studyen_US
dc.typeArticleen_US

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