Carvacrol mitigates Mercury chloride induced neurotoxicity by regulation of NRF-2/HO-1/NF-κB expression

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dc.contributor.authorAkaras, Nurhan
dc.contributor.authorŞimşek, Hasan
dc.contributor.authorİleritürk, Mustafa
dc.contributor.authorKüçükler, Sefa
dc.contributor.authorGür, Cihan
dc.contributor.authorKandemir, Fatih Mehmet
dc.date.accessioned2025-09-17T05:32:42Z
dc.date.available2025-09-17T05:32:42Z
dc.date.issued2025
dc.departmentTıp Fakültesi
dc.description.abstractMercury chloride (HgCl2) is an environmental pollutant that has serious toxic effects on the central nervous system. Carvacrol (CRV), which has phytotherapeutic, pharmacological, biological, and aromatic properties, has neuroprotective effects. The aim of this study was to investigate the possible neuroprotective effect of CRV on HgCl2-induced central neurotoxicity in rats. In the study, HgCl2 (1.23 mg/kg) and CRV (25 or 50 mg/kg) alone or their combinations were administered to rats for 7 days. Then, the proteins and pathological changes specific to autophagy, apoptosis, inflammation and oxidative stress processes in the brain tissue were analyzed by biochemical, molecular, histological and immunohistochemical methods. It was determined that CRV treatment significantly increased antioxidant enzyme (catalase, superoxide dismutase and glutathione peroxidase) activities and non-enzymatic (glutathione) antioxidants while reducing HgCl2-induced lipid peroxidation. In addition, it was determined that Nrf-2, HO-1, NQO1 mRNA transcript levels, which are among the oxidative stress parameters of CRV administration, increased. It was observed that HgCl2 increased the expression of NF-κB, TNF-α, IL-1β, iNOS and nNOS cytokines and Rage, STAT3, NLRP3, MAPK14, MAPK15 and JNK, whereas CRV treatment suppressed these genes. In this study, it was determined that HgCl2 induces apoptotic (caspase-3, Bax, Bcl-2) and autophagic (Beclin-1) markers, whereas CRV can protect brain tissues from the destructive effect of H HgCl2 by showing anti-apoptotic and anti-autophagic. In addition, decreased Akt-2 and Foxo1 expression and increased GFAP levels in HgCl2-induced brain tissue were regulated after CRV administration. The H&E staining results showed that CRV preserved the histological architecture and integrity of the cerebral cortex. The findings of this study indicate that CRV has neuropreventive potential against HgCl2-induced neurotoxicity by reducing oxidative stress, inflammation, apoptosis and autophagy.
dc.identifier.doi10.1016/j.jtemb.2025.127715
dc.identifier.issn0946672X
dc.identifier.issue-
dc.identifier.scopus2-s2.0-105013093954
dc.identifier.scopusqualityQ2
dc.identifier.urihttps://doi.org/10.1016/j.jtemb.2025.127715
dc.identifier.urihttps://hdl.handle.net/20.500.12451/14426
dc.identifier.volume91
dc.indekslendigikaynakScopus
dc.institutionauthorAkaras, Nurhan
dc.institutionauthorŞimşek, Hasan
dc.institutionauthorKandemir, Fatih Mehmet
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.subjectCarvacrol
dc.subjectMercury Chloride
dc.subjectBrain
dc.subjectNeuroinflammation
dc.subjectOxidative Stress
dc.titleCarvacrol mitigates Mercury chloride induced neurotoxicity by regulation of NRF-2/HO-1/NF-κB expression
dc.typeArticle

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