Vitamin D mitigates cisplatin-mediated acute kidney injury through modulation of NRF2/HO-1 and autophagy signaling pathways

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dc.contributor.authorYildiz, Azibe
dc.contributor.authorTanbek, Kevser
dc.contributor.authorCuglan, Songul
dc.contributor.authorKoca, Gokce
dc.contributor.authorAkyuz, Mustafa
dc.contributor.authorVardi, Nigar
dc.date.accessioned2026-04-04T13:34:50Z
dc.date.available2026-04-04T13:34:50Z
dc.date.issued2026
dc.departmentİnönü Üniversitesi
dc.description.abstractThis study investigated the effects of vitamin D (Vit D) pretreatment on renal oxidative stress in cisplatin (CP)induced acute kidney injury (AKI). Twenty-one six-month-old female Wistar albino rats (277.3 +/- 11.8 g) were randomly divided into three groups (n = 7): Control, CP, and Vit D+CP. The control group received intraperitoneal 0.9% NaCl for 7 days. The CP group received a single intraperitoneal dose of CP (7 mg/kg) on day 1 of the experiment. The Vit D+CP group received a single intraperitoneal dose of CP (7 mg/kg) on day 1, followed by daily intraperitoneal Vit D (1000 IU/mL) for 7 consecutive days. The oxidative stress index (OSI) of kidney tissue was calculated based on total antioxidant status (TAS) and total oxidant status (TOS) measurements. Furthermore, tissue samples were assessed histologically and immunohistochemically for NRF2, HO-1, BECN1, LC3B, and vimentin proteins. CP, which significantly increased the OSI values and the immunoreactivity of NRF2, HO1, BECN1, LC3B, and vimentin, caused moderate-to-severe tubular damage histopathologically (P < 0.05). By contrast, the OSI was lower in the Vit D+CP group (P < 0.05). Tubular damage was significantly reduced in this group, and NRF2, HO-1, BECN1, LC3B, and vimentin immunoreactivity were also remarkably lower compared with the CP group (P < 0.05). In conclusion, the findings of the present study suggest that Vit D may exert a protective effect against CP-induced AKI. Vit D supplementation during CP chemotherapy may potentially mitigate renal adverse effects; however, further experimental and clinical studies are required to validate these findings.
dc.identifier.doi10.1016/j.tice.2026.103440
dc.identifier.issn0040-8166
dc.identifier.orcid0009-0002-9147-0253
dc.identifier.pmid41806633
dc.identifier.scopus2-s2.0-105032492004
dc.identifier.scopusqualityQ3
dc.identifier.urihttps://doi.org/10.1016/j.tice.2026.103440
dc.identifier.urihttps://hdl.handle.net/11616/109418
dc.identifier.volume101
dc.identifier.wosWOS:001715853800001
dc.identifier.wosqualityQ1
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherChurchill Livingstone
dc.relation.ispartofTissue & Cell
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_WOS_20250329
dc.subjectAcute kidney injury
dc.subjectAutophahgy
dc.subjectCisplatin
dc.subjectNRF2/HO-1
dc.subjectOxidative status
dc.subjectVitamin D
dc.titleVitamin D mitigates cisplatin-mediated acute kidney injury through modulation of NRF2/HO-1 and autophagy signaling pathways
dc.typeArticle

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