The lung endothelin system: a potent therapeutic target with bosentan for the amelioration of lung alterations in a rat model of diabetes mellitus

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dc.contributor.authorCayir, A.
dc.contributor.authorUgan, R. A.
dc.contributor.authorAlbayrak, A.
dc.contributor.authorKose, D.
dc.contributor.authorAkpinar, E.
dc.contributor.authorCayir, Y.
dc.contributor.authorKara, M.
dc.date.accessioned2020-06-25T18:12:55Z
dc.date.available2020-06-25T18:12:55Z
dc.date.issued2015
dc.departmentKırıkkale Üniversitesi
dc.descriptionCayir, Yasemin/0000-0001-9133-5460; Albayrak, Abdulmecit/0000-0002-1062-1965; UGAN, RUSTEM ANIL/0000-0002-4837-2343; ATMACA, HASAN TARIK/0000-0001-8379-4114
dc.description.abstractPurpose The aim of this study is to show the effect of a new mechanism on endothelin (ET) receptors in the physiopathology of diabetes-related pulmonary injury. We tested the hypothesis that dual ET-1 receptor antagonism via bosentan can reverse diabetes-induced lung injury. Methods The rats (24 male) were separated into four groups: group 1 (HEALTHY): Control group; group 2 (DM): Streptozotocin 60 mg/kg (i.p.); group 3 (DM + BOS1): Diabetes + bosentan 50 mg/kg per-os; group 4 (DM + BOS-2): Diabetes + bosentan 100 mg/kg per-os. The bosentan treatment was initiated immediately after the onset of STZ-induced diabetes and continued for 6 weeks. Results In the treatment group, SOD activity was significantly increased, although GSH and MDA levels and TNF-alpha and TGF-beta gene expression were decreased. Bosentan 50 mg/kg and bosentan 100 mg/kg showed a significantly down-regulatory effect on ET-1, ET-A, and ET-B mRNA expression. Conclusions In conclusion, increased endothelin levels in the lung associated with diabetes may be one cause of endothelial dysfunction, cytokine increase, and oxidant/antioxidant imbalance in the pathogenesis of complications that may develop during diabetes. With its multiple effects, bosentan therapy may be an effective option against complications that may develop in association with diabetes.en_US
dc.identifier.citationclosedAccessen_US
dc.identifier.doi10.1007/s40618-015-0282-y
dc.identifier.endpage998en_US
dc.identifier.issn0391-4097
dc.identifier.issn1720-8386
dc.identifier.issue9en_US
dc.identifier.pmid25847324
dc.identifier.scopus2-s2.0-84940046823
dc.identifier.scopusqualityQ1
dc.identifier.startpage987en_US
dc.identifier.urihttps://doi.org/10.1007/s40618-015-0282-y
dc.identifier.urihttps://hdl.handle.net/20.500.12587/6075
dc.identifier.volume38en_US
dc.identifier.wosWOS:000362680700008
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherSpringeren_US
dc.relation.ispartofJournal Of Endocrinological Investigation
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectBosentanen_US
dc.subjectLung injuryen_US
dc.subjectEndothelin systemen_US
dc.subjectDiabetesen_US
dc.titleThe lung endothelin system: a potent therapeutic target with bosentan for the amelioration of lung alterations in a rat model of diabetes mellitusen_US
dc.typeArticle

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