Ceftriaxone ameliorates cyclosporine A-induced oxidative nephrotoxicity in rat

dc.contributor.authorYilmaz, Nigar
dc.contributor.authorIlhan, Selcuk
dc.contributor.authorNaziroglu, Mustafa
dc.contributor.authorOktar, Suleyman
dc.contributor.authorNacar, Ahmet
dc.contributor.authorArica, Vefik
dc.contributor.authorTutanc, Murat
dc.date.accessioned2026-08-12T17:14:30Z
dc.date.issued2011
dc.departmentFırat Üniversitesi
dc.description.abstractA growing body of evidence now suggested that cyclosporine A (CycA)-induced nephrotoxicity is a crucial clinical problem and oxidative stress is importantly responsible for its toxicity. Ceftriaxone induced antioxidant effect in brain and neuronal tissues against oxidative damage although its antioxidant potential effect on kidney has not been clarified. The aim of this study was to evaluate whether ceftriaxone protects CycA-induced oxidative stress kidney injury in rats. Twenty-four rats were equally divided into four groups. First group was used as control. Ceftriaxone (200 mg/kg) and CycA (15 mg/kg) were administrated to second and third groups for 10 days, respectively. The ceftriaxone and CycA combination was given to rats constituting the fourth group for 10 days. Lipid peroxidation (LP), urea nitrogen and lactate dehydrogenase (LDH) levels were higher in CycA group than in control and ceftriaxone groups although LP, urea nitrogen and LDH levels were lower in ceftriaxone + CycA group than in control and ceftriaxone groups. Glutathione peroxidase and catalase activities were lower in CycA group than in control whereas their activities were increased in control and ceftriaxone groups. Superoxide dismutase activity did not change by the treatments. Ceftriaxone administration recovered also CycA-induced atrophy, vacuolization and exfoliations of tubular epithelium and glomerular collapse in histopathological evaluation of kidney. In conclusion, we observed that ceftriaxone is beneficial on CycA-induced oxidative stress in kidney of rats by modulating oxidative and antioxidant system. Copyright (C) 2011 John Wiley & Sons, Ltd.
dc.identifier.doi10.1002/cbf.1727
dc.identifier.endpage107
dc.identifier.issn0263-6484
dc.identifier.issn1099-0844
dc.identifier.issue2
dc.identifier.orcid0000-0003-0151-5981
dc.identifier.orcid0000-0001-6274-5700
dc.identifier.orcid0000-0003-0887-6974
dc.identifier.pmid21287576
dc.identifier.scopus2-s2.0-79952226945
dc.identifier.scopusqualityQ3
dc.identifier.startpage102
dc.identifier.urihttps://doi.org/10.1002/cbf.1727
dc.identifier.urihttps://hdl.handle.net/11508/51853
dc.identifier.volume29
dc.identifier.wosWOS:000288079400004
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherWiley
dc.relation.ispartofCell Biochemistry and Function
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_WoS_20260511
dc.subjectceftriaxone
dc.subjectcyclosporine A
dc.subjectnephrotoxicity
dc.subjectoxidative stress
dc.subjectglutathione peroxidase
dc.subjecthistology
dc.subjectkidney
dc.titleCeftriaxone ameliorates cyclosporine A-induced oxidative nephrotoxicity in rat
dc.typeArticle

Dosyalar