The ameliorative effect of carvacrol on sodium arsenite-induced hepatotoxicity in rats: Possible role of Nrf2/HO-1, RAGE/NLRP3, Bax/Bcl-2/Caspase-3, and Beclin-1 pathways

dc.authorid0000-0003-3936-4146
dc.authorid0000-0001-6775-7858
dc.authorid0000-0002-4581-4492
dc.authorid0000-0002-8222-5515
dc.authorid0000-0002-8457-9448
dc.authorid0000-0001-5573-4923
dc.authorid0000-0002-8490-2479
dc.contributor.authorGencer, Selman
dc.contributor.authorGür, Cihan
dc.contributor.authorİleritürk, Mustafa
dc.contributor.authorKüçükler, Sefa
dc.contributor.authorAkaras, Nurhan
dc.contributor.authorŞimşek, Hasan
dc.contributor.authorKandemir, Fatih M.
dc.date.accessioned2024-11-13T13:20:18Z
dc.date.available2024-11-13T13:20:18Z
dc.date.issued2024
dc.departmentTıp Fakültesi
dc.description.abstractArsenic is a toxic environmental pollutant heavy metal, and one of its critical target tissues in the body is the liver. Carvacrol is a natural phytocompound that stands out with its antioxidant, anti-inflammatory, and antiapoptotic properties. The current study aims to investigate the protective feature of carvacrol against sodium arsenite-induced liver toxicity. Thirty-five Sprague-Dawley male rats were divided into five groups: Control, Sodium arsenite (SA), CRV, SA + CRV25, and SA + CRV50. Sodium arsenite was administered via oral gavage at a dose of 10 mg/kg for 14 days, and 30 min later, CRV 25 or 50 mg/kg was administered via oral gavage. Oxidative stress, inflammation, apoptosis, autophagy damage pathways parameters, and liver tissue integrity were analyzed using biochemical, molecular, western blot, histological, and immunohistological methods. Carvacrol decreased sodium arsenite-induced oxidative stress by suppressing malondialdehyde levels and increasing superoxide dismutase, catalase, glutathione peroxidase activities, and glutathione levels. Carvacrol reduced inflammation damage by reducing sodium arsenite-induced increased levels of NF-?B and the cytokines (TNF-?, IL-1?, IL-6, RAGE, and NLRP3) it stimulates. Carvacrol also reduced sodium arsenite-induced autophagic (Beclin-1, LC3A, and LC3B) and apoptotic (P53, Apaf-1, Casp-3, Casp-6, Casp-9, and Bax) parameters. Carvacrol preserved sodium arsenite-induced impaired liver tissue structure. Carvacrol alleviated toxic damage by reducing sodium arsenite-induced increases in oxidative stress, inflammation, apoptosis, and autophagic damage parameters in rat liver tissues. Carvacrol was also beneficial in preserving liver tissue integrity.
dc.identifier.doi10.1002/jbt.23863
dc.identifier.issn1095-6670
dc.identifier.issue10en_US
dc.identifier.scopusqualityQ2
dc.identifier.urihttps:/dx.doi.org/10.1002/jbt.23863
dc.identifier.urihttps://hdl.handle.net/20.500.12451/12628
dc.identifier.volume38en_US
dc.identifier.wosqualityN/A
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
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.subjectAutophagy
dc.subjectCarvacrol
dc.subjectInflammation
dc.subjectOxidative Stress
dc.subjectSodium Arsenite
dc.titleThe ameliorative effect of carvacrol on sodium arsenite-induced hepatotoxicity in rats: Possible role of Nrf2/HO-1, RAGE/NLRP3, Bax/Bcl-2/Caspase-3, and Beclin-1 pathways
dc.typeArticle

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