Neuroprotective effects of melatonin upon the offspring cerebellar cortex in the rat model of BCNU-induced cortical dysplasia

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dc.contributor.authorUyanikgil, Yigit
dc.contributor.authorBaka, Meral
dc.contributor.authorAtes, Utku
dc.contributor.authorTurgut, Mehmet
dc.contributor.authorYavasoglu, Altug
dc.contributor.authorUelker, Sibel
dc.contributor.authorSoezmen, Eser Yildirim
dc.contributor.authorSezer, Ebru
dc.contributor.authorElmas, Cigdem
dc.contributor.authorYurtseven, Mine Ertem
dc.date.accessioned2019-10-27T19:33:22Z
dc.date.available2019-10-27T19:33:22Z
dc.date.issued2007
dc.departmentEge Üniversitesien_US
dc.description.abstractCortical dysplasia is a malformation characterized by defects in proliferation, migration and maturation. This study was designed to evaluate the alterations in offspring rat cerebellum induced by maternal exposure to carmustine-[1,3-bis (2-chloroethyl)-1-nitrosoure] (BCNU) and to investigate the effects of exogenous melatonin upon cerebellar BCNU-induced cortical dysplasia, using histological and biochemical analyses. Pregnant Wistar rats were assigned to five groups: intact-control, saline-control, melatonin-treated, BCNU-exposed and BCNU-exposed plus melatonin. Rats were exposed to BCNU on embryonic day 15 and melatonin was given until delivery. Immuno/histochemistry and electron microscopy were carried out on the offspring cerebellum, and levels of malondialdehyde and superoxide dismutase were determined. Histopathologic ally, typical findings were observed in the cerebella from the control groups, but the findings consistent with early embryonic development were noted in BCNU-exposed cortical dysplasia group. There was a marked increase in the number of TUNEL positive cells and nestin positive cells in BCNU-exposed group, but a decreased immunoreactivity to glial fibrillary acidic protein, synaptophysin and transforming growth factor beta 1 was observed, indicating a delayed maturation, and melatonin significantly reversed these changes. Malondialdehyde level in BCNU-exposed group was higher than those in control groups and melatonin decreased malondialdehyde levels in BCNU group (P<0.01), while there were no significant differences in the superoxide dismutase levels between these groups. These data suggest that exposure of animals to BCNU during pregnancy leads to delayed maturation of offspring cerebellum and melatonin protects the cerebellum against the effects of BCNU. (C) 2007 Elsevier B.V. All rights reserved.en_US
dc.identifier.doi10.1016/j.brainres.2007.05.025en_US
dc.identifier.endpage144en_US
dc.identifier.issn0006-8993
dc.identifier.pmid17572393en_US
dc.identifier.scopusqualityN/Aen_US
dc.identifier.startpage134en_US
dc.identifier.urihttps://doi.org/10.1016/j.brainres.2007.05.025
dc.identifier.urihttps://hdl.handle.net/11454/39460
dc.identifier.volume1160en_US
dc.identifier.wosWOS:000248658500014en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherElsevier Science Bven_US
dc.relation.ispartofBrain Researchen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectcortical dysplasiaen_US
dc.subjectpregnancyen_US
dc.subjectmelatoninen_US
dc.subjectraten_US
dc.subjectcerebellumen_US
dc.subjectoffspringen_US
dc.titleNeuroprotective effects of melatonin upon the offspring cerebellar cortex in the rat model of BCNU-induced cortical dysplasiaen_US
dc.typeArticleen_US

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