Targeting different pathophysiological events after traumatic brain injury in mice: Role of melatonin and memantine

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dc.authorid0000-0001-6494-8923
dc.authorid0000-0002-9704-6173
dc.authorid0000-0002-6242-3709
dc.authorid0000-0002-9476-8488
dc.authorid0000-0002-6895-8560
dc.authorid0000-0002-5072-132X
dc.authorid0000-0002-1064-7989
dc.contributor.authorKeleştemur, Taha
dc.contributor.authorYuluğ, Burak
dc.contributor.authorÇağlayan, Ahmet Burak
dc.contributor.authorBeker, Mustafa Çağlar
dc.contributor.authorKılıç, Ülkan
dc.contributor.authorÇağlayan, Berrak
dc.contributor.authorYalçın, Esra
dc.contributor.authorGündoğdu, Reyhan Zeynep
dc.contributor.authorKılıç, Ertuğrul
dc.date.accessioned10.07.201910:49:13
dc.date.accessioned2019-07-10T20:02:02Z
dc.date.available10.07.201910:49:13
dc.date.available2019-07-10T20:02:02Z
dc.date.issued2016
dc.departmentİstanbul Medipol Üniversitesi, Rektörlük, Rejeneratif ve Restoratif Tıp Araştırmaları Merkezi (REMER)
dc.departmentİstanbul Medipol Üniversitesi, Tıp Fakültesi, Dahili Tıp Bilimleri Bölümü, Nöroloji Ana Bilim Dalı
dc.departmentİstanbul Medipol Üniversitesi, Tıp Fakültesi, Temel Tıp Bilimleri Bölümü, Tıbbi Biyoloji Ana Bilim Dalı
dc.descriptionWOS: 000369471900016
dc.descriptionPubMed ID: 26639427
dc.description.abstractThe tissue damage that emerges during traumatic brain injury (TBI) is a consequence of a variety of pathophysiological events, including free radical generation and over-activation of N-methyl-D-aspartate-type glutamate receptors (NMDAR). Considering the complex pathophysiology of TBI, we hypothesized that combination of neuroprotective compounds, targeting different events which appear during injury, may be a more promising approach for patients. In this context, both NMDAR antagonist memantine and free radical scavenger melatonin are safe in humans and promising agents for the treatment of TBI. Herein, we examined the effects of melatonin administered alone or in combination with memantine on the activation of signaling pathways, injury development and DNA fragmentation. Both compounds reduced brain injury moderately and the density of DNA fragmentation significantly. Notably, melatonin/memantine combination decreased brain injury and DNA fragmentation significantly, which was associated with reduced p38 and ERK-1/2 phosphorylation. As compared with melatonin and memantine groups, SAM/INK-1/2 phosphorylation was also reduced in melatonin/memantine combined animals. In addition, melatonin, memantine and their combination decreased iNOS activity significantly. Here, we provide evidence that melatonin/memantine combination protects brain from traumatic injury, which was associated with decreased DNA fragmentation, p38 phosphorylation and iNOS activity.
dc.description.sponsorshipEMBO (European Molecular Biology Organization); Turkish Academy of Sciences (TUBA)en_US
dc.description.sponsorshipThis work was supported by EMBO (European Molecular Biology Organization) installation grant and Turkish Academy of Sciences (TUBA).en_US
dc.identifier.citationKeleştemur, T., Yuluğ, B., Çağlayan, A. B., Beker, M. Ç., Kılıç, Ü., Çağlayan, B., Yalçın, E., Gündoğdu, R. Z. ve Kılıç, E. (2016). Targeting different pathophysiological events after traumatic brain injury in mice: Role of melatonin and memantine. Neuroscience Letters, 612, 92-97. https://dx.doi.org/10.1016/j.neulet.2015.11.043
dc.identifier.doi10.1016/j.neulet.2015.11.043
dc.identifier.endpage97
dc.identifier.issn0304-3940
dc.identifier.issn1872-7972
dc.identifier.scopusqualityQ2
dc.identifier.startpage92
dc.identifier.urihttps://dx.doi.org/10.1016/j.neulet.2015.11.043
dc.identifier.urihttps://hdl.handle.net/20.500.12511/3527
dc.identifier.volume612
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherElsevier Ireland Ltd
dc.relation.ispartofNeuroscience Lettersen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/embargoedAccess
dc.subjectMemantine
dc.subjectMelatonin
dc.subjectTraumatic Brain Injury
dc.subjectDNA fragmentation
dc.titleTargeting different pathophysiological events after traumatic brain injury in mice: Role of melatonin and memantine
dc.typeArticle

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