Urotensin receptor antagonist palosuran attenuates cyclosporine-a-induced nephrotoxicity in rats

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dc.contributor.authorOlukman, Murat
dc.contributor.authorCan, Cenk
dc.contributor.authorCoskunsever, Deniz
dc.contributor.authorUyanikgil, Yigit
dc.contributor.authorCavusoglu, Turker
dc.contributor.authorSozmen, Eser
dc.contributor.authorUlker, Sibel
dc.date.accessioned2020-12-01T12:09:10Z
dc.date.available2020-12-01T12:09:10Z
dc.date.issued2019
dc.departmentEge Üniversitesien_US
dc.descriptionCavusoglu, Turker/0000-0001-7100-7080; uyanikgil, Yigit/0000-0002-4016-0522; Kozcu, Fatma Gul/0000-0003-1304-8065; uyanikgil, Yigit/0000-0002-4016-0522en_US
dc.description.abstractBackground. Cyclosporine-A (CsA) is widely used for immunosuppressivetherapy in renal transplantation. Nephrotoxicity is the main dose-limiting undesirable consequence of CsA. Urotensin II (U-II), a novel peptide with a powerful influence on vascular biology, has been added to the list of potential renal vascular regulators. Upregulation of the urotensin receptors and elevation of plasma U-II levels are thought to possibly play a role in the etiology of renal failure. Objectives. the present study examines this hypothesis by evaluating renal function and histology with regard to the potential role of U-II and its antagonist, palosuran, in the pathogenesis of CsA-induced nephrotoxicity in rats. Material and methods. Male Sprague-Dawley rats were treated with CsA (15 mg/kg, for 21 days, intraperitoneally) or CsA + palosuran (300 mg/kg, for 21 days). Renal function was measured and histopathology, U-II immunostaining and protein detection with western blotting of the kidneys were performed. Results. Cyclosporine-A administration caused a marked decline in creatinine clearance (Ccr). Fractional sodium excretion (FENa) tended to increase in the CsA-treated rats. Plasma U-II levels decreased in the CsA-treated rats. Cyclosporine-A treatment resulted in a marked deterioration in renal histology and an increase in the expression of U-II protein in the kidneys. Palosuran's improvement of renal function manifested as a significant decrease in serum creatinine levels and a significant increase in urine creatinine levels, resulting in a marked increase in Ccr. Palosuran produced a significant normalization of kidney histology and prevented an increase in U-II expression. Conclusions. Cyclosporine-A-induced renal impairment was accompanied by an increase in U-II expression in kidneys and a contrary decrease in systemic U-II levels. Palosuran improved the condition of rats suffering from renal dysfunction by preventing the decrease in renal U-II expression without affecting the systemic levels of U-II. the protective effect of palosuran in CsA nephrotoxicity is possibly independent of its U-II receptor antagonism.en_US
dc.identifier.doi10.17219/acem/104544en_US
dc.identifier.endpage1401en_US
dc.identifier.issn1899-5276
dc.identifier.issue10en_US
dc.identifier.pmid31518496en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage1393en_US
dc.identifier.urihttps://doi.org/10.17219/acem/104544
dc.identifier.urihttps://hdl.handle.net/11454/63342
dc.identifier.volume28en_US
dc.identifier.wosWOS:000493904000014en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherWroclaw Medical Univen_US
dc.relation.ispartofAdvances in Clinical and Experimental Medicineen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectnephrotoxicityen_US
dc.subjecturotensin-IIen_US
dc.subjectcyclosporine-Aen_US
dc.subjectpalosuranen_US
dc.subjectexperimenten_US
dc.titleUrotensin receptor antagonist palosuran attenuates cyclosporine-a-induced nephrotoxicity in ratsen_US
dc.typeArticleen_US

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