Dietary Carvacrol Attenuates Cyclophosphamide-Induced Neurotoxicity: Implications for Food-Derived Neuroprotection and Molecular Mechanisms

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dc.authorid0000-0001-6193-3734
dc.contributor.authorKizil, Hamit Emre
dc.date.accessioned2026-02-28T12:17:40Z
dc.date.available2026-02-28T12:17:40Z
dc.date.issued2025
dc.departmentBayburt Üniversitesi
dc.description.abstractCarvacrol (CRV) is a phenolic monoterpene abundant in culinary herbs such as oregano and thyme and is well known for its potent antioxidant, anti-inflammatory, and neuroprotective properties. This study investigated the ability of CRV to counteract neurotoxicity induced by cyclophosphamide (CP), a widely used antineoplastic agent. Male Wistar albino rats were divided into five groups and received CP and/or CRV treatments. Neurotoxicity and neuroprotection were evaluated through biochemical assays, real-time PCR, histopathological and immunohistochemical analyses, and behavioral testing (Morris Water Maze). CP administration led to significant increases in oxidative stress markers, disruption of antioxidant enzyme activities, upregulation of inflammatory mediators (NF-kappa B, TNF-alpha, iNOS), dysregulation of apoptotic regulators (increased Bax and Casp-3, decreased Bcl-2), alterations in autophagy markers (Beclin-1, LC3A, LC3B), and suppression of Notch1/Hes1 signaling. Histopathological analyses revealed neuronal degeneration, vascular hyperemia, and increased GFAP and 8-OHdG expression in brain tissue. CRV treatment, particularly at higher doses, effectively mitigated these biochemical, molecular, and histological alterations. Notably, CRV administration preserved spatial learning and memory function in CP-treated rats, as demonstrated by the Morris Water Maze test, indicating functional neuroprotection. These findings highlight the multifaceted neuroprotective mechanisms of CRV and suggest its potential as a food-derived bioactive compound for development into functional foods or dietary supplements to improve the quality of life for cancer patients undergoing chemotherapy.
dc.identifier.doi10.1002/fsn3.70734
dc.identifier.issn2048-7177
dc.identifier.issue8
dc.identifier.pmid40777202
dc.identifier.scopus2-s2.0-105012753137
dc.identifier.scopusqualityQ1
dc.identifier.urihttps://doi.org/10.1002/fsn3.70734
dc.identifier.urihttps://hdl.handle.net/20.500.12403/5908
dc.identifier.volume13
dc.identifier.wosWOS:001559319600011
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherWiley
dc.relation.ispartofFood Science & Nutrition
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_WoS_20260218
dc.subjectapoptosis
dc.subjectautophagy
dc.subjectcarvacrol
dc.subjectcyclophosphamide
dc.subjectneuroinflammation
dc.subjectneurotoxicity
dc.subjectoxidative stress
dc.titleDietary Carvacrol Attenuates Cyclophosphamide-Induced Neurotoxicity: Implications for Food-Derived Neuroprotection and Molecular Mechanisms
dc.typeArticle

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