Dexpanthenol protects against nicotine-induced kidney injury by reducing oxidative stress and apoptosis through activation of the AKT/Nrf2/HO-1 pathway

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dc.authoridUremis, Muhammed Mehdi/0000-0003-2296-2422
dc.authoridTaslidere, Elif/0000-0003-1723-2556
dc.authorwosidUremis, Muhammed Mehdi/HKP-0531-2023
dc.authorwosidTaslidere, Elif/ABI-8046-2020
dc.contributor.authorUremis, Muhammed Mehdi
dc.contributor.authorGurel, Elif
dc.contributor.authorAslan, Meral
dc.contributor.authorTaslidere, Elif
dc.date.accessioned2024-08-04T20:54:37Z
dc.date.available2024-08-04T20:54:37Z
dc.date.issued2024
dc.departmentİnönü Üniversitesien_US
dc.description.abstractDexpanthenol (DEX), a subtype of vitamin B5, plays an important role in anabolic reactions, cellular energy and regeneration in the body. Nicotine has been shown to induce kidney damage through the mechanisms of oxidative stress and apoptosis. The purpose of this study was to investigate the potential protective effects of DEX against nicotine-induced kidney damage through modulation of the AKT/Nrf2/HO-1 signaling pathway. Male rats were intraperitoneally administered with 0.5 mg/kg/day nicotine and/or 500 mg/kg/day DEX for 8 weeks. Following administration, renal function tests were conducted on serum samples, and histopathological examinations and analysis of oxidative stress markers and antioxidant enzymes were performed on tissue samples. Protein levels of Akt, Nrf-2, HO-1, Bcl-xL, and Caspase-9 were also evaluated. Nicotine administration resulted in decreased protein levels of p-Akt, Nrf-2, HO-1, and Bcl-xL and increased Caspase-9 protein levels. In addition, nicotine administration caused an increase in MDA, TOS, and OSI levels and a decrease in GSH, GSH-Px, GST, CAT, SOD, and TAS levels. Additionally, BUN and Creatinine levels increased after nicotine administration. DEX administration positively regulated these parameters and brought them closer to control levels. Nicotine-induced kidney injury caused apoptosis and oxidative stress through Caspase-9 activation. DEX effectively prevented nicotine-induced kidney damage by increasing intracellular antioxidant levels and regulating apoptosis through Bcl-xL activation. These findings suggest that DEX has potential as a protective agent against nicotine-induced kidney damage.en_US
dc.description.sponsorshipBayer Turk Chemical Industryen_US
dc.description.sponsorshipAcknowledgementsThe authors are very thankful to Bayer Turk Chemical Industry for supplying the Dexpanthenol substance for the proposed research works.en_US
dc.identifier.doi10.1007/s00210-023-02671-7
dc.identifier.endpage1114en_US
dc.identifier.issn0028-1298
dc.identifier.issn1432-1912
dc.identifier.issue2en_US
dc.identifier.pmid37606756en_US
dc.identifier.scopus2-s2.0-85168564118en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage1105en_US
dc.identifier.urihttps://doi.org/10.1007/s00210-023-02671-7
dc.identifier.urihttps://hdl.handle.net/11616/101528
dc.identifier.volume397en_US
dc.identifier.wosWOS:001052448200002en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherSpringeren_US
dc.relation.ispartofNaunyn-Schmiedebergs Archives of Pharmacologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectNicotineen_US
dc.subjectDexpanthenolen_US
dc.subjectKidneyen_US
dc.subjectAKTen_US
dc.subjectNrf2en_US
dc.subjectHO-1 signaling pathwayen_US
dc.subjectApoptosisen_US
dc.subjectCaspaseen_US
dc.subjectBcl-XLen_US
dc.subjectOxidative stressen_US
dc.titleDexpanthenol protects against nicotine-induced kidney injury by reducing oxidative stress and apoptosis through activation of the AKT/Nrf2/HO-1 pathwayen_US
dc.typeArticleen_US

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