Pretreatment with Paricalcitol Attenuates Oxidative Stress in Renal lschemia Reperfusion-Induced Nephropathy in Rats

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dc.contributor.authorAydin, Fatma Yilmaz
dc.contributor.authorYilmaz, Zulfukar
dc.contributor.authorYildirim, Yasar
dc.contributor.authorAydin, Emre
dc.contributor.authorKetani, Aydin
dc.contributor.authorBahadir, Veysi
dc.contributor.authorKaplan, Ibrahim
dc.date.accessioned2024-04-24T17:44:44Z
dc.date.available2024-04-24T17:44:44Z
dc.date.issued2020
dc.departmentDicle Üniversitesien_US
dc.description.abstractOBJECTIVE: To investigate whether paricalcitol could ameliorate kidney injury due to ischemia reperfusion (I/R) in an experimental study. STUDY DESIGN: Rats were divided into 4 groups: control, paricalcitol, I/R, and paricalcitol +I/R, each containing 7 animals. Intraperitoneal 0.3 mu g/kg paricalcitol was administered to rats once a day for 5 consecutive days in the paricalcitol and paricalcitol+1/R groups. After right nephrectomy, rats were exposed to ischemia/ reperfusion on day 6 in the paricalcitol+1/R and I/R groups. Oxidant and antioxidant parameters, kidney function tests, and histology were investigated. RESULTS: Serum urea and creatinine levels exhibited a significant decrease in rats treated with paricalcitol before I/R as compared to rats exposed just to I/R. In a comparison of the paricalcitol +1/R group with the I/R group, serum total oxidant status (TOS) levels decreased significantly; serum total antioxidant capacity (TAC) and nitric oxide levels, however, increased significantly with paricalcitol administration. Malondialdehyde and TOS levels of kidney tissue were significantly lower, whereas TAC and paraoxonase levels were higher in the paricalcitol +I/R group than in the I/R group. Renal tissue injury scores were found to be significantly higher in the I/R group than in the paricalcitol+ I/R group. CONCLUSION: Pretreatment with paricalcitol was detected to be renoprotective by decreasing renal injury related with renal I/R, which was assessed by improved renal function and histopathologii.en_US
dc.description.sponsorshipDicle University Research Foundation [13-TF-58]en_US
dc.description.sponsorshipThis study was supported by Dicle University Research Foundation (Reference Number: 13-TF-58).en_US
dc.identifier.endpage60en_US
dc.identifier.issn0884-6812
dc.identifier.issue2en_US
dc.identifier.startpage54en_US
dc.identifier.urihttps://hdl.handle.net/11468/22262
dc.identifier.volume42en_US
dc.identifier.wosWOS:000548509900004
dc.identifier.wosqualityQ4
dc.indekslendigikaynakWeb of Science
dc.language.isoenen_US
dc.publisherSci Printers & Publ Incen_US
dc.relation.ispartofAnalytical and Quantitative Cytopathology and Histopathology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectAcute Kidney Injuryen_US
dc.subjectAntioxidantsen_US
dc.subjectDisease Modelsen_US
dc.subjectAnimalen_US
dc.subjectIschemia-Reperfusion Injuryen_US
dc.subjectKidneyen_US
dc.subjectOxidative Stressen_US
dc.subjectParicalcitolen_US
dc.subjectRatsen_US
dc.subjectSprague-Dawleyen_US
dc.subjectReperfusion Injuryen_US
dc.titlePretreatment with Paricalcitol Attenuates Oxidative Stress in Renal lschemia Reperfusion-Induced Nephropathy in Ratsen_US
dc.titlePretreatment with Paricalcitol Attenuates Oxidative Stress in Renal lschemia Reperfusion-Induced Nephropathy in Rats
dc.typeArticleen_US

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