Neuroprotective effects of amantadine for experimental acute carbon monoxide poisoning

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dc.contributor.authorZengin, E.N.
dc.contributor.authorKayır, S.
dc.contributor.authorDo?an, G.
dc.contributor.authorZengin, M.
dc.contributor.authorEkici, A. Akdağlı
dc.contributor.authorYalvaç, M.
dc.contributor.authorAyaz, E.
dc.contributor.authorÖzcan, O.
dc.contributor.authorKaraca, O.
dc.contributor.authorYa?an, Ö.
dc.contributor.authorAlagöz, A.
dc.date.accessioned2023-01-16T11:47:25Z
dc.date.available2023-01-16T11:47:25Z
dc.date.issued2022
dc.departmentTıp Fakültesi
dc.description.abstractAmantadine is known to have a neuroprotective effect in many neurological diseases. This study aims at investigating the neuroprotective effect of amantadine in rats exposed to carbon monoxide (CO) poisoning. MATERIALS AND METHODS: Rats were maintained under standard experimental laboratory conditions and randomized into 4 different groups of 7 each namely control, amantadine only, CO exposure, and amantadine + CO exposure. For immunohistochemical analysis, tissues taken from the prefrontal and hippocampal regions were taken into formalin and kept for at least one day. Afterward, the tissue was followed and blocked for paraffin blocking. N-Methyl D-Aspartate (NMDA) levels in homogenates were studied by the Enzyme-Linked Immunosorbent Assay (ELISA) method. Superoxide dismutase (SOD) and catalase (CAT) activities in the supernatants were studied with commercial kits. Nitric oxide (NO) and Asymmetric Dimethyl Arginine (ADMA) levels were studied by the ELISA method. Enzyme activity values were calculated by dividing the protein values in the supernatants and normalizing them. RESULTS: CAT, SOD, NMDA, ADMA, and NO levels were statistically significantly different between the groups (p < 0.05). According to post-hoc pairwise comparison test results, the values of the control and amantadine groups for CAT, SOD, NMDA, ADMA, and NO parameters were significantly higher than that of CO group. Similarly, values in the control and amantadine groups were considerably higher than values for the amantadine + CO group. NMDA values were significantly lower in group amantadine + CO than in CO group (p: 0.049). CONCLUSIONS: Apoptosis and endothelial damage after CO poisoning is a complex process, and amantadine administration has a limited contribution in preventing this process.
dc.identifier.doi10.26355/eurrev_202210_29872
dc.identifier.endpage6927en_US
dc.identifier.issn1128-3602
dc.identifier.issue19en_US
dc.identifier.pmid36263571
dc.identifier.scopusqualityQ2
dc.identifier.startpage6919en_US
dc.identifier.urihttps:/dx.doi.org/10.26355/eurrev_202210_29872
dc.identifier.urihttps://hdl.handle.net/20.500.12451/9941
dc.identifier.volume26en_US
dc.identifier.wosWOS:000877188200007
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.language.isoen
dc.publisherVerduci Editore s.r.l
dc.relation.ispartofEuropean Review for Medical and Pharmacological Sciences
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsAttribution-NonCommercial-NoDerivs 3.0 United States*
dc.rightsinfo:eu-repo/semantics/embargoedAccess
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/us/*
dc.subjectAmantadine
dc.subjectBcl-2
dc.subjectCarbon Monoxide
dc.subjectIntoxication
dc.subjectN-Metil D-Aspartate
dc.subjectNeuroprotective
dc.subjectPoisoning
dc.subjectRat
dc.titleNeuroprotective effects of amantadine for experimental acute carbon monoxide poisoning
dc.typeArticle

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