Phosphodiesterase type 5 inhibition attenuates cyclosporine A induced nephrotoxicity in mice

dc.contributor.authorEssiz, D.
dc.contributor.authorSozmen, M.
dc.contributor.authorSudagidan, M.
dc.contributor.authorDevrim, A. K.
dc.date.accessioned2020-06-25T18:13:25Z
dc.date.available2020-06-25T18:13:25Z
dc.date.issued2015
dc.departmentKırıkkale Üniversitesi
dc.description.abstractWe investigated the renal protective effects of phophodiesterase type 5 (PDE5) inhibitors in mice with cyclosporine A (CyA; a calcineurin phosphatase inhibitor) induced nephrotoxicity. Fifty male mice were divided into five groups of 10. Group 1 received no treatment, group 2 received only saline orally, group 3 received 30 mg/kg/day CyA by subcutaneous injection, group 4 received only 30 mg/kg/day vardenafil orally, and group 5 received 30 mg/kg/day CyA by subcutaneous injection and 30 mg/kg/day vardenafil orally. At 28 days, platelet-derived growth factor A (PDGF-A) and C (PDGF-C), transforming growth factor-beta 1 (TGF-beta 1), cyclo-oxygenase 1 and 2 (COX-1 and COX-2), and P glycoprotein (Pgp) expression levels were measured in the renal tissues. In addition, expressions of COX-1 and COX-2 genes were determined using real-time PCR. PDE5 inhibitor administration ameliorated decreased PDGF-A and C, TGF-beta 1, COX-1 and -2, and Pgp expression levels by modulation of cyclic guanosine monophosphate (cGMP) activity in kidneys. The relative expressions of COX-1 and COX-2 genes to GAPDH revealed that the maximum increase was obtained in the group treated with CyA and vardenafil for both COX-1 and COX-2 genes. Our study revealed that long term oral treatment with vardenafil protects kidneys from CyA induced nephrotoxicity. We showed that long term oral treatment with PDE5 prevents pathological kidney changes caused by CyA induced nephrotoxicity.en_US
dc.description.sponsorshipScientific and Technological Research Council of Turkey (TUBITAK-TOVAG), Ankara, TurkeyTurkiye Bilimsel ve Teknolojik Arastirma Kurumu (TUBITAK) [110 O 402]en_US
dc.description.sponsorshipOur study was funded by the Scientific and Technological Research Council of Turkey (TUBITAK-TOVAG; Project no. 110 O 402), Ankara, Turkey.en_US
dc.identifier.citationclosedAccessen_US
dc.identifier.doi10.3109/10520295.2014.976270
dc.identifier.endpage178en_US
dc.identifier.issn1052-0295
dc.identifier.issn1473-7760
dc.identifier.issue3en_US
dc.identifier.pmid25420893
dc.identifier.scopus2-s2.0-84964292253
dc.identifier.scopusqualityQ2
dc.identifier.startpage167en_US
dc.identifier.urihttps://doi.org/10.3109/10520295.2014.976270
dc.identifier.urihttps://hdl.handle.net/20.500.12587/6192
dc.identifier.volume90en_US
dc.identifier.wosWOS:000352110200002
dc.identifier.wosqualityQ4
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherTaylor & Francis Incen_US
dc.relation.ispartofBiotechnic & Histochemistry
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectcyclosporine Aen_US
dc.subjectimmunohistochemistryen_US
dc.subjectnephrotoxicityen_US
dc.subjectphosphodiesterase type 5en_US
dc.titlePhosphodiesterase type 5 inhibition attenuates cyclosporine A induced nephrotoxicity in miceen_US
dc.typeArticle

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