Protective effects of molsidomine against doxorubicin-induced renal damage in rats

dc.contributor.authorOguz, Fatih
dc.contributor.authorBeytur, Ali
dc.contributor.authorSarihan, Ediz
dc.contributor.authorOguz, Hilal K.
dc.contributor.authorBentli, Recep
dc.contributor.authorSamdanci, Emine
dc.contributor.authorEkinci, Nihat
dc.date.accessioned2026-08-12T17:04:43Z
dc.date.issued2016
dc.departmentFırat Üniversitesi
dc.description.abstractPurpose: The purpose of this study was to investigate the therapeutic and protective effects of molsidomine (MLS) against doxorubicin (DOX)-induced renal damage in rats. Methods: Forty rats were randomly divided into five groups (control, MLS, DOX, DOX+MLS and MLS+DOX groups). Thiobarbituric acid reactive substance (TBARS), reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), nitric oxide (NO) and glutathione peroxidase (GPx) levels were determined from kidney tissues and blood urea nitrogen (BUN), creatinine (Cr) and albumin (Alb) levels also determined. Results: DOX treatment caused a significant increase in TBARS levels and a significant decrease in the GSH and CAT levels compared with the control group. In comparison, MLS administration before DOX injection caused a significant decrease in TBARS levels and also increases in GSH and CAT levels, whereas treatment of MLS after DOX injection did not show any beneficial effect on these parameters. All groups showed a significant increase in NO levels compared to the control group. There were no significant differences among the all groups for BUN and Cr levels. Serum level of Alb decreased in the DOX-treated groups when compared with control and MLS groups. The histopathological findings were in accordance with the biochemical results. MLS treatment reversed the DOX-induced kidney damage in group 4. MLS treatment before DOX injection exerted a protective effect against DOX-induced kidney damage. Conclusions: MLS shows promise as a possible therapeutic intervention for the prevention of kidney injury associated with DOX treatment. Additional studies are warranted.
dc.identifier.endpageE14
dc.identifier.issn0147-958X
dc.identifier.issn1488-2353
dc.identifier.issue1
dc.identifier.orcid0000-0001-9497-3468
dc.identifier.orcid0000-0002-5608-9003
dc.identifier.orcid0000-0002-6920-3856
dc.identifier.pmid26833172
dc.identifier.scopus2-s2.0-85009968291
dc.identifier.scopusqualityQ2
dc.identifier.startpageE7
dc.identifier.urihttps://hdl.handle.net/11508/48836
dc.identifier.volume39
dc.identifier.wosWOS:000369142400002
dc.identifier.wosqualityQ4
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherCanadian Soc Clinical Investigation
dc.relation.ispartofClinical and Investigative Medicine
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_WoS_20260511
dc.subjectIschemia-Reperfusion Injury
dc.subjectAcid Phenethyl Ester
dc.subjectNitric-Oxide
dc.subjectInduced Nephrotoxicity
dc.subjectToxicity
dc.subjectCardiomyopathy
dc.subjectAminoguanidine
dc.subjectGlutathione
dc.subjectInhibition
dc.subjectApoptosis
dc.titleProtective effects of molsidomine against doxorubicin-induced renal damage in rats
dc.typeArticle

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