Protective Effects of Chrysin Against Diclofenac-Induced Nephrotoxicity in Rats via Attenuation of Oxidative Stress, Apoptosis and Endoplasmic Reticulum Stress

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dc.authorid0000-0001-5608-554X
dc.authorid0000-0003-0418-6773
dc.authorid0000-0001-6775-7858
dc.authorid0000-0001-6801-6242
dc.contributor.authorÇağlayan, Cüneyt
dc.contributor.authorEkinci, İzzettin
dc.contributor.authorGür, Cihan
dc.contributor.authorAyna, Adnan
dc.contributor.authorBayav, İbrahim
dc.contributor.authorKandemir, Fatih Mehmet
dc.date.accessioned2025-07-09T12:15:47Z
dc.date.available2025-07-09T12:15:47Z
dc.date.issued2025
dc.departmentTıp Fakültesi
dc.description.abstractDiclofenac (DCL) is a broadly prescribed non-steroidal anti-inflammatory drug (NSAID) for pain management and has been linked to nephrotoxicity despite its therapeutic benefits. This study provides new insights into the palliative impacts of chrysin (CH) against DCL-induced kidney damage by modulating oxidative injury, endoplasmic reticulum (ER) stress and apoptosis. The rats were divided into five groups: the control group (Group 1), CH-only group (50 mg/kg, Group 2), DCL-only group (50 mg/kg, Group 3), DCL + CH (25 mg/kg, Group 4), and DCL + CH (50 mg/kg, Group 5). DCL injection led to significant renal damage marked by elevated serum urea, creatinine and malondialdehyde (MDA) levels, reduced glutathione (GSH) concentration, and decreased activities of antioxidant enzymes (glutathione peroxidase, superoxide dismutase and catalase). The mRNA expression levels of Ho-1 and Nrf2 were also suppressed. Additionally, DCL treatment triggered apoptosis as evidenced by increased expression of Bax and caspase-3 alongside decreased Bcl-2 expression. Furthermore, DCL induced ER stress was confirmed by upregulation of Perk, Ire1, Atf-6, and Grp78 transcription levels. Also, it was demonstrated that DCL treatment upregulated Mmp2 and Mmp9 levels. Treatment with CH significantly mitigated these adverse effects suggesting that CH effectively protects DCL-induced kidney toxicity by targeting multiple pathways. In summary, this study highlights the importance of CH as a promising therapeutic agent for alleviating kidney damage associated with DCL toxicity.
dc.identifier.doi10.1002/jbt.70373
dc.identifier.issn10956670
dc.identifier.issue6
dc.identifier.pmid40534331
dc.identifier.scopus105008864030
dc.identifier.urihttps://dx.doi.org/10.1002/jbt.70373
dc.identifier.urihttps://hdl.handle.net/20.500.12451/13229
dc.identifier.volume39
dc.identifier.wosWOS:001511056500001
dc.identifier.wosqualityQ2
dc.indekslendigikaynakPubMed
dc.indekslendigikaynakScopus
dc.indekslendigikaynakWeb of Science
dc.institutionauthorKandemir, Fatih Mehmet
dc.language.isoen
dc.publisherJohn Wiley and Sons Inc
dc.relation.ispartofJournal of Biochemical and Molecular Toxicology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectApoptosis
dc.subjectChrysin
dc.subjectDiclofenac
dc.subjectEndoplasmic Reticulum Stress
dc.subjectNephrotoxicity
dc.titleProtective Effects of Chrysin Against Diclofenac-Induced Nephrotoxicity in Rats via Attenuation of Oxidative Stress, Apoptosis and Endoplasmic Reticulum Stress
dc.typeArticle

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