Dexpanthenol exhibits antiapoptotic and anti-inflammatory effects against nicotine-induced liver damage by modulating Bax/Bcl-xL, Caspase-3/9, and Akt/NF-?B pathways

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dc.authoridTaslidere, Elif/0000-0003-1723-2556
dc.authoridUremis, Nuray/0000-0002-3958-4352
dc.authorwosidTaslidere, Elif/ABI-8046-2020
dc.contributor.authorUremis, Nuray
dc.contributor.authorAslan, Meral
dc.contributor.authorTaslidere, Elif
dc.contributor.authorGurel, Elif
dc.date.accessioned2024-08-04T20:54:58Z
dc.date.available2024-08-04T20:54:58Z
dc.date.issued2024
dc.departmentİnönü Üniversitesien_US
dc.description.abstractChronic tobacco use can lead to liver damage and inflammation due to the accumulation of various toxins in the body. This study aimed to investigate the correlation between the molecular mechanisms of nicotine-induced liver injury, the caspase cascade, and the Akt/NF-kappa B signaling pathway, as well as the protective effects of dexpanthenol (DEX). Male rats were subjected to intraperitoneal injections of nicotine at a concentration of 0.5 mg/kg/day and/or DEX at a concentration of 500 mg/kg/day for 8 weeks. After the treatment period, liver function tests were conducted on serum samples, and tissue samples were analyzed for protein levels of Akt, NF-kappa B, Bax, Bcl-xL, Caspase-3, and Caspase-9, along with histopathological changes. Additionally, assessments of oxidative stress markers and proinflammatory cytokines were carried out. Nicotine administration led to elevated levels of IL-6, IL-1 beta, MDA, TOS, and oxidative stress index, accompanied by decreased TAS levels. Moreover, nicotine exposure reduced the p-Akt/Akt ratio, increased NF-kappa B, Bax, Caspase-3, and Caspase-9 protein levels, and decreased the antiapoptotic protein Bcl-xL levels. DEX treatment significantly mitigated these effects, restoring the parameters to levels comparable to those of the control group. Nicotine-induced liver injury resulted in oxidative stress, inflammation, and apoptosis, mediated by Bax/Bcl-xL, Caspase-3, Caspase-9, and Akt/NF-kappa B pathways. Conversely, DEX effectively attenuated nicotine-induced liver injury by modulating apoptosis through NF-kappa B, Caspase-3, Caspase-9, Bax inhibition, and Bcl-xL activation. Chronic nicotine exposure led to oxidative stress, inflammation, and apoptosis, as evidenced by altered protein levels in Bax/Bcl-xL, Caspase-3/9, and Akt/NF-kappa B pathways. Dexpanthenol treatment effectively countered these effects, highlighting its potential as a therapeutic agent for nicotine-related liver injury.imageen_US
dc.identifier.doi10.1002/jbt.23622
dc.identifier.issn1095-6670
dc.identifier.issn1099-0461
dc.identifier.issue1en_US
dc.identifier.pmid38229321en_US
dc.identifier.scopus2-s2.0-85181526825en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.urihttps://doi.org/10.1002/jbt.23622
dc.identifier.urihttps://hdl.handle.net/11616/101757
dc.identifier.volume38en_US
dc.identifier.wosWOS:001134997700001en_US
dc.identifier.wosqualityN/Aen_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherWileyen_US
dc.relation.ispartofJournal of Biochemical and Molecular Toxicologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectapoptosisen_US
dc.subjectBcl-2 familyen_US
dc.subjectcaspaseen_US
dc.subjectdexpanthenolen_US
dc.subjectinflammationen_US
dc.subjectliveren_US
dc.subjectnicotineen_US
dc.subjectoxidative stressen_US
dc.titleDexpanthenol exhibits antiapoptotic and anti-inflammatory effects against nicotine-induced liver damage by modulating Bax/Bcl-xL, Caspase-3/9, and Akt/NF-?B pathwaysen_US
dc.typeArticleen_US

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