Please use this identifier to cite or link to this item: http://hdl.handle.net/11452/28279
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dc.contributor.authorÇetinkaya, Merih-
dc.contributor.authorTayman, Cüneyt-
dc.contributor.authorÇekmez, Ferhat-
dc.contributor.authorCanpolat, Fuat Emre-
dc.contributor.authorTunç, Turan-
dc.contributor.authorSarıcı, S. Ümit-
dc.date.accessioned2022-08-19T08:08:47Z-
dc.date.available2022-08-19T08:08:47Z-
dc.date.issued2013-07-
dc.identifier.citationÇetinkaya, M. vd. (2013). "Cytidine 5 '-diphosphocholine ameliorates hyperoxic lung injury in a neonatal rat model". Pediatric Research, 74(1), 26-33.en_US
dc.identifier.issn0031-3998-
dc.identifier.urihttps://doi.org/10.1038/pr.2013.68-
dc.identifier.urihttps://www.nature.com/articles/pr201368-
dc.identifier.urihttp://hdl.handle.net/11452/28279-
dc.description.abstractBACKGROUND: Bronchopulmonary dysplasia (BPD) is an important cause of morbidity. The aim of this study was to evaluate the preventive effect of cytidine 5'-diphosphocholine (CDP-choline) treatment on hyperoxic lung injury in a neonatal rat model. METHODS: A total of 30 newborn pups were divided into control, hyperoxia, and hyperoxia + CDP-choline groups. After birth, pups in the control group were kept in room air and received saline injections, whereas those in hyperoxia and hyperoxia + CDP-choline groups were exposed to 95% O-2 and received daily injections of saline and CDP-choline throughout postnatal day 10, respectively. Histopathological scoring, radial alveolar count, lamellar body membrane protein expression, fibrosis, proinflammatory cytokine levels, lung tissue and bronchoalveolar lavage (BAL) fluid phospholipid content, and apoptosis were evaluated. RESULTS: Hyperoxia-induced severe lung damage was reduced significantly by CDP-choline treatment. Radial alveolar count and lamellar body membrane protein expression were significantly recovered, and the number of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling-positive cells, active caspase-3 expression, and tissue proinflammatory cytokine levels were decreased by CDP-choline administration. Lung tissue and BAL phospholipid contents showed significant increases after COP-choline administration. CONCLUSION: These data show that COP-choline ameliorates hyperoxic lung injury in a neonatal rat model. It may therefore be suggested that CDP-choline may be a novel therapeutic option for the prevention of BPD.en_US
dc.language.isoenen_US
dc.publisherSpringernatureen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.rightsAtıf Gayri Ticari Türetilemez 4.0 Uluslararasıtr_TR
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectPediatricsen_US
dc.subjectNicotinic acetylcholine-receptoren_US
dc.subjectAutonomic nervous-systemen_US
dc.subjectBronchopulmonary dysplasiaen_US
dc.subjectPreterm infantsen_US
dc.subjectCdp-cholineen_US
dc.subjectDisaturated phosphatidylcholineen_US
dc.subjectSurfactanten_US
dc.subjectInflammationen_US
dc.subjectApoptosisen_US
dc.subjectPulmonaryen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnimals, newbornen_US
dc.subject.meshCytidine diphosphate cholineen_US
dc.subject.meshDisease models, animalen_US
dc.subject.meshHyperoxiaen_US
dc.subject.meshLung injuryen_US
dc.subject.meshRatsen_US
dc.titleCytidine 5 '-diphosphocholine ameliorates hyperoxic lung injury in a neonatal rat modelen_US
dc.typeArticleen_US
dc.identifier.wos000321795300005tr_TR
dc.identifier.scopus2-s2.0-84880291831tr_TR
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergitr_TR
dc.contributor.departmentUludağ Üniversitesi/Tıp Fakültesi/Anatomi Anabilim Dalı.tr_TR
dc.contributor.departmentUludağ Üniversitesi/Tıp Fakültesi/Farmakoloji Anabilim Dalı.tr_TR
dc.identifier.startpage26tr_TR
dc.identifier.endpage33tr_TR
dc.identifier.volume74tr_TR
dc.identifier.issue1tr_TR
dc.relation.journalPediatric Researchen_US
dc.contributor.buuauthorCansev, Mehmet-
dc.contributor.buuauthorKafa, İlker Mustafa-
dc.contributor.researcheridM-9071-2019tr_TR
dc.contributor.researcheridAAG-7125-2021tr_TR
dc.relation.collaborationYurt içitr_TR
dc.identifier.pubmed23598810tr_TR
dc.subject.wosPediatricsen_US
dc.indexed.wosSCIEen_US
dc.indexed.scopusScopusen_US
dc.indexed.pubmedPubMeden_US
dc.wos.quartileQ1en_US
dc.contributor.scopusid8872816100tr_TR
dc.contributor.scopusid8450193200tr_TR
dc.subject.scopusCiticoline; Brain Ischemia; Glycerylphosphorylcholineen_US
dc.subject.emtreeCaspase 3en_US
dc.subject.emtreeCiticolineen_US
dc.subject.emtreeCytokineen_US
dc.subject.emtreeDNA nucleotidylexotransferaseen_US
dc.subject.emtreeInterleukin 1betaen_US
dc.subject.emtreeInterleukin 6en_US
dc.subject.emtreeMembrane proteinen_US
dc.subject.emtreePhospholipiden_US
dc.subject.emtreeTumor necrosis factor alphaen_US
dc.subject.emtreeAnimal cellen_US
dc.subject.emtreeAnimal experimenten_US
dc.subject.emtreeAnimal modelen_US
dc.subject.emtreeAnimal tissueen_US
dc.subject.emtreeAntiinflammatory activityen_US
dc.subject.emtreeApoptosisen_US
dc.subject.emtreeArticleen_US
dc.subject.emtreeControlled studyen_US
dc.subject.emtreeCytokine productionen_US
dc.subject.emtreeDrug efficacyen_US
dc.subject.emtreeDrug mechanismen_US
dc.subject.emtreeEnzyme activationen_US
dc.subject.emtreeHistopathologyen_US
dc.subject.emtreeHyperoxiaen_US
dc.subject.emtreeLamellar bodyen_US
dc.subject.emtreeLipid peroxidationen_US
dc.subject.emtreeLung fibrosisen_US
dc.subject.emtreeLung fluiden_US
dc.subject.emtreeLung homogenateen_US
dc.subject.emtreeLung injuryen_US
dc.subject.emtreeLung lavageen_US
dc.subject.emtreeLung parenchymaen_US
dc.subject.emtreeNewbornen_US
dc.subject.emtreeNonhumanen_US
dc.subject.emtreePerinatal perioden_US
dc.subject.emtreePriority journalen_US
dc.subject.emtreeProphylaxisen_US
dc.subject.emtreeProtein blood levelen_US
dc.subject.emtreeProtein expressionen_US
dc.subject.emtreeRaten_US
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