Tnf-alpha inhibition by infliximab as a new target for the prevention of glycerol-contrast-induced nephropathy

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dc.contributor.authorSaritemur, Murat
dc.contributor.authorUn, Harun
dc.contributor.authorCadirci, Elif
dc.contributor.authorKarakus, Emre
dc.contributor.authorAkpinar, Erol
dc.contributor.authorHalici, Zekai
dc.contributor.authorAtmaca, Hasan Tarik
dc.date.accessioned2020-06-25T18:13:34Z
dc.date.available2020-06-25T18:13:34Z
dc.date.issued2015
dc.departmentKırıkkale Üniversitesi
dc.descriptionKaraman, Adem/0000-0002-3091-0609; UGAN, RUSTEM ANIL/0000-0002-4837-2343; UN, Harun/0000-0003-1772-282X; ATMACA, HASAN TARIK/0000-0001-8379-4114
dc.description.abstractContrast medium-induced nephropathy (CIN) remains as a problem with high incidence and mortality rates. The aim of this study is to examine the roles of infliximab (INF) in the glycerol (GLY) and CIN model in rats. The rats were separated into five groups (n=8): Healthy, GLY, GLY+CM, GLY+CM+INF 5 mg/kg intraperitoneally (i.p.), and GLY+CM+INF 7 mg/kg (i.p.). Antioxidant levels in the therapy groups were observed to be quite similar to those in the healthy group. In this study, while the kidney TNF-alpha, TGF-1 beta and Caspase 3 gene expressions' levels increased in the nephrotoxic groups, these levels were found to have decreased in the treatment groups. Moreover, histopathologic examination showed that hyaline, haemorrhagic casts and necrosis were increased in nephrotoxicity group, whereas they decreased in the therapy group. Furthermore, TNF-alpha and NF-kappa B expression were decreased with infliximab administrated groups similar to control group. In conclusion, we suggest that infliximab have protective roles on CIN. (C) 2015 Elsevier B.V. All rights reserved.en_US
dc.description.sponsorshipAtaturk University Scientific Experimental Project OfficeAtaturk University [2013/54]en_US
dc.description.sponsorshipThis article was supported by the Ataturk University Scientific Experimental Project Office, Project Number: 2013/54en_US
dc.identifier.citationclosedAccessen_US
dc.identifier.doi10.1016/j.etap.2015.01.002
dc.identifier.endpage588en_US
dc.identifier.issn1382-6689
dc.identifier.issn1872-7077
dc.identifier.issue2en_US
dc.identifier.pmid25682004
dc.identifier.scopus2-s2.0-84922572118
dc.identifier.scopusqualityQ1
dc.identifier.startpage577en_US
dc.identifier.urihttps://doi.org/10.1016/j.etap.2015.01.002
dc.identifier.urihttps://hdl.handle.net/20.500.12587/6223
dc.identifier.volume39en_US
dc.identifier.wosWOS:000353929900011
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherElsevier Science Bven_US
dc.relation.ispartofEnvironmental Toxicology And Pharmacology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectContrast-mediaen_US
dc.subjectNephrotoxicityen_US
dc.subjectInfliximaben_US
dc.subjectRaten_US
dc.titleTnf-alpha inhibition by infliximab as a new target for the prevention of glycerol-contrast-induced nephropathyen_US
dc.typeArticle

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