Zingerone reduces sodium arsenite-induced nephrotoxicity by regulating oxidative stress, inflammation, apoptosis and histopathological changes

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dc.contributor.authorAkaras, Nurhan
dc.contributor.authorGür, Cihan
dc.contributor.authorKüçükler, Sefa
dc.contributor.authorKandemir, Fatih Mehmet
dc.date.accessioned2023-02-28T06:29:26Z
dc.date.available2023-02-28T06:29:26Z
dc.date.issued2023
dc.departmentTıp Fakültesi
dc.description.abstractArsenic is widely available in the environment and arsenic toxicity is a public health problem of serious concern worldwide. Zingerone is a promising phytochemical with various pharmacological effects. In this study, the potential protective effect of zingerone against sodium arsenite (NaAsO2, SA) induced nephrotoxicity was investigated. Thirty-five male Sprague-Dawley rats were divided into five different groups as control, zingerone, SA, SA + zingerone 25, SA + zingerone 50. SA was administered alone at a dose of 10 mg/kg for 14 days or given 30 min before zingerone (25 mg/kg or 50 mg/kg) treatment. At the end of the experiment, the kidney tissues was examined biochemically, molecularly and microscopically. SA toxicity was associated with increased malondialdehyde level, whereas glutathione, superoxide dismutase, catalase, and glutathione peroxidase were decreased. Administration of SA caused inflammation in the kidney tissue by upregulation of NF-?B and IL-1?, TNF-?, IL-6, iNOS, COX-2, MAPK14, MAPK15, JNK. SA administration caused apoptosis in the kidney by upregulating caspase-3 and Bax levels and downregulating Bcl-2, and autophagy by activating beclin-1. Also, SA administration showed a suppressive effect on AKT2 and FOXO1 mRNA transcript levels. All these factors impair kidney function and increase creatinine and urea levels, resulting in pathological changes and a decrease in nephrin. Treatment with zingerone at doses of 25 and 50 mg/kg significantly reduced oxidative stress, inflammation, apoptosis and autophagy in kidney tissue. In addition, it was confirmed by histological evaluation as well as serum urea and creatinine levels that kidney damage due to SA toxicity can be modulated by zingerone administration.
dc.identifier.doi10.1016/j.cbi.2023.110410
dc.identifier.pmid36822304
dc.identifier.scopusqualityQ1
dc.identifier.urihttps:/dx.doi.org/10.1016/j.cbi.2023.110410
dc.identifier.urihttps://hdl.handle.net/20.500.12451/10305
dc.identifier.volume374en_US
dc.identifier.wosWOS:000994649300001
dc.identifier.wosqualityQ1
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherElsevier
dc.relation.ispartofChemico-Biological Interactions
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectApoptosis
dc.subjectInflammation
dc.subjectNephrotoxicity
dc.subjectOxidative Stress
dc.subjectSodium Arsenite
dc.subjectZingerone
dc.titleZingerone reduces sodium arsenite-induced nephrotoxicity by regulating oxidative stress, inflammation, apoptosis and histopathological changes
dc.typeArticle

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