The possible role of interleukin-33 as a new player in the pathogenesis of contrast-induced nephropathy in diabetic rats

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dc.contributor.authorDemirtas, Levent
dc.contributor.authorTurkmen, Kultigin
dc.contributor.authorKandemir, Fatih Mehmet
dc.contributor.authorOzkaraca, Mustafa
dc.contributor.authorKucukler, Sefa
dc.contributor.authorGurbuzel, Mehmet
dc.contributor.authorComakli, Selim
dc.date.accessioned2024-02-23T14:34:36Z
dc.date.available2024-02-23T14:34:36Z
dc.date.issued2016
dc.departmentNEÜen_US
dc.description.abstractIntroduction: Patients with diabetic kidney disease (DKD) are more prone to contrast-induced nephropathy (CN). Apoptosis and autophagy were found to be essential in the pathogenesis of DKD. Interleukin-33 (IL-33) is a cytokine, but its role in DKD and CN is unknown. As IL-33 is modulated by apoptosis, we aimed to determine the relationship between IL-33 apoptosis and autophagy in DKD with CN. Materials and methods: Thirty male Sprague-Dawley rats were enrolled and randomly allocated into three groups. The first group was comprised of healthy rats (HRs), whereas the other two groups were made up of diabetic rats (DRs) and diabetic rats with CN (DRs+CN). All groups except the HRs received 50mg/kg/day of streptozotocin (STZ). The DRs+CN group was induced by administering 1.5mg/kg of intravenous radiocontrast dye on the 35th day. Results: We observed increased IL-33 in the kidney tissue following induction of CN in the DRs. The DRs showed moderate immunopositivity, and the DRs+CN showed severe immunopositivity for caspase-3, cleaved caspase-3, caspase-8, caspase-9, LC3B, and Beclin-1 in tubular cells and glomeruli. The DRs also showed moderate immunopositivity in tubular cells, and the DRs+CN group showed severe immunopositivity for IL-33 in tubular cells. Increased caspase-3 was found in both glomeruli and tubuli; however, we could not demonstrate IL-33 in glomeruli. This could be secondary to inactivation of IL-33 via increased caspase-3 activity. Conclusion: The release of IL-33 from necrotic cells might induce autophagy, which can further balance the effects of increased apoptosis secondary to CN in DKD.en_US
dc.identifier.doi10.3109/0886022X.2016.1165034
dc.identifier.endpage960en_US
dc.identifier.issn0886-022X
dc.identifier.issn1525-6049
dc.identifier.issue6en_US
dc.identifier.pmid27055881en_US
dc.identifier.scopus2-s2.0-84964054253en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage952en_US
dc.identifier.urihttps://doi.org/10.3109/0886022X.2016.1165034
dc.identifier.urihttps://hdl.handle.net/20.500.12452/15663
dc.identifier.volume38en_US
dc.identifier.wosWOS:000379778100015en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherTaylor & Francis Ltden_US
dc.relation.ispartofRenal Failureen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectApoptosisen_US
dc.subjectAutophagyen_US
dc.subjectContrast-Induced Nephropathyen_US
dc.subjectDiabetic Kidney Diseaseen_US
dc.subjectInterleukin-33en_US
dc.titleThe possible role of interleukin-33 as a new player in the pathogenesis of contrast-induced nephropathy in diabetic ratsen_US
dc.typeArticleen_US

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