Zingerone ameliorates sodium arsenite-induced cardiotoxicity in rats by suppressing oxidative stress and inflammation via Nrf2 /GCLM\GCLC signaling pathways

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dc.contributor.authorKandemir, Özge
dc.contributor.authorKandemir, Fatih Mehmet
dc.contributor.authorAkaras, Nurhan
dc.contributor.authorKüçükler, Sefa
dc.contributor.authorGür, Cihan
dc.contributor.authorİleritürk, Mustafa
dc.contributor.authorŞimşek, Hasan
dc.contributor.authorGül, Murat
dc.date.accessioned2025-09-17T07:26:35Z
dc.date.available2025-09-17T07:26:35Z
dc.date.issued2025
dc.departmentTeknik Bilimler Meslek Yüksekokulu
dc.description.abstractArsenic toxicity is a serious threat to human health, transmitted through many factors in the environment, especially water and contaminated food. Epidemiologic studies have reported that arsenite increases mortality and morbidity by causing cardiac damage, but the mechanism of action on cardiotoxicity remains to be elucidated. Zingerone (ZNG) obtained from ginger root is a monomer with pharmacological effects such as antioxidant, anti-inflammatory, and anticancer. This study was conducted to investigate the protective potential of zingerone against sodium arsenite-induced cardiac damage in rats. Sodium arsenite (SA) (10 mg/kg) was administered to rats for 14 days to induce cardiotoxicity, while zingerone (25 and 50 mg/kg) was administered for treatment. Then, oxidative stress markers, inflammatory factors, and apoptosis-related proteins were evaluated by molecular and biochemical methods. It was also supported by histological and immunohistochemical stainings. According to the results, ZNG treatment significantly reduced SA-induced altered cardiac functions. Compared with the SA group, rats co-treated with SA and ZNG showed a significant decrease in oxidant markers and an increase in antioxidant levels. Additionally, ZNG treatment regulated the expression of NRF2, HO-1, NQO1, GCLM, and GCLC genes related to oxidative stress. Moreover, treatment with ZNG significantly inhibited arsenite-induced apoptosis (p53, Apaf-1, Bax, Bcl-2, Casp-3, Casp-6, Casp-9) while reducing the levels of inflammatory mediators including NF-κB, TNF-α, IL-1β, COX-2 and iNOS in cardiac tissue. Finally, co-administration of ZNG with SA reduced SA-induced cardiac histopathological changes in rats. The results of this study suggest that ZNG may provide an alternative for clinical inflammation control through antioxidant and anti-inflammatory activities. © 2025 Elsevier GmbH
dc.identifier.doi10.1016/j.jtemb.2025.127716
dc.identifier.issn0946672X
dc.identifier.scopus2-s2.0-105012894903
dc.identifier.scopusqualityQ2
dc.identifier.urihttps://doi.org/10.1016/j.jtemb.2025.127716
dc.identifier.urihttps://hdl.handle.net/20.500.12451/14432
dc.identifier.volume91
dc.indekslendigikaynakScopus
dc.institutionauthorKandemir, Özge
dc.institutionauthorKandemir, Fatih Mehmet
dc.institutionauthorAkaras, Nurhan
dc.institutionauthorŞimşek, Hasan
dc.institutionauthorGül, Murat
dc.institutionauthorid0000-0001-8884-4168
dc.language.isoen
dc.publisherElsevier GmbH
dc.relation.ispartofJournal of Trace Elements in Medicine and Biology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectSodium Arsenite
dc.subjectZingerone
dc.subjectCardiotoxicity
dc.subjectOxidative Stress
dc.subjectInflammation
dc.titleZingerone ameliorates sodium arsenite-induced cardiotoxicity in rats by suppressing oxidative stress and inflammation via Nrf2 /GCLM\GCLC signaling pathways
dc.typeArticle

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