Multi-Pathway Renoprotection by Betanin Against Docetaxel Nephrotoxicity: Modulation of Inflammation, ER Stress, Apoptosis, and Ferroptosis

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dc.contributor.authorCelbek, Busra Suzen
dc.contributor.authorAkaras, Nurhan
dc.contributor.authorSimsek, Hasan
dc.contributor.authorMutlu, Huseyin
dc.contributor.authorKizil, Hamit Emre
dc.contributor.authorKandemir, Ozge
dc.contributor.authorKandemir, Fatih Mehmet
dc.date.accessioned2026-09-01T15:53:10Z
dc.date.available2026-09-01T15:53:10Z
dc.date.issued2026
dc.departmentBayburt Üniversitesi
dc.description.abstractDocetaxel (DTX), a cornerstone chemotherapeutic agent, has its clinical utility significantly limited by dose-dependent nephrotoxicity. This study investigated the multi-pathway renoprotective mechanisms of betanin (BTN), a natural antioxidant derived from beetroot, against DTX-induced kidney injury. Male Wistar rats received DTX (30 mg/kg, i.p., single dose) with or without BTN (100 mg/kg/day, p.o.) for 7 days. DTX induced severe renal dysfunction with elevated serum urea and creatinine, and significant oxidative stress characterized by increased MDA and decreased GSH, GPx, SOD, and CAT. Molecular analysis demonstrated widespread upregulation of pro-inflammatory (NF-kappa B, TNF-alpha, IL-1 beta), endoplasmic reticulum stress (PERK, ATF6), pro-apoptotic (Caspase-3, Bax, Apaf-1), and pro-ferroptotic (PTGS2, TfR1) mediators, with concurrent downregulation of protective Bcl-2 and GPx4. Histopathological examination revealed extensive tubular injury, while immunohistochemical analysis showed markedly increased kidney injury marker KIM-1 and decreased aquaporin-1 expression. Remarkably, BTN co-administration significantly attenuated all biochemical, molecular, and structural derangements, restored tissue architecture, and normalized KIM-1 and AQP-1 expression. In conclusion, betanin provides robust, multi-pathway renoprotection against docetaxel-induced nephrotoxicity by concurrently targeting oxidative stress, inflammation, ER stress, apoptosis, and ferroptosis.
dc.identifier.doi10.1002/jbt.71007
dc.identifier.issn1095-6670
dc.identifier.issn1099-0461
dc.identifier.issue7
dc.identifier.orcid0000-0001-8884-4168
dc.identifier.pmid42402965
dc.identifier.scopus2-s2.0-105043896733
dc.identifier.scopusqualityQ2
dc.identifier.urihttp://dx.doi.org/10.1002/jbt.71007
dc.identifier.urihttps://hdl.handle.net/20.500.12403/8570
dc.identifier.volume40
dc.identifier.wosWOS:001811201300001
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherWiley
dc.relation.ispartofJournal of Biochemical and Molecular Toxicology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_WOS_20260820
dc.subjectApoptosis
dc.subjectBetanin
dc.subjectDocetaxel
dc.subjectFerroptosis
dc.subjectOxidative Stress
dc.titleMulti-Pathway Renoprotection by Betanin Against Docetaxel Nephrotoxicity: Modulation of Inflammation, ER Stress, Apoptosis, and Ferroptosis
dc.typeArticle

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