Investigating the effects of carvacrol in isoproterenol-induced myocardial injury: Role of H-FABP and Gal-3/TLR4/MYD88/NF-κB signaling pathway modulation

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dc.contributor.authorKüçükler, Sefa
dc.contributor.authorÇomaklı, Selim
dc.contributor.authorÖzdemir, Selçuk
dc.contributor.authorDeğirmençay, Şükrü
dc.contributor.authorKandemir, Fatih Mehmet
dc.contributor.authorGenç, Aydın
dc.contributor.authorDalkılınç, Elif
dc.contributor.authorAydın, Şeyma
dc.date.accessioned2025-09-19T06:41:53Z
dc.date.available2025-09-19T06:41:53Z
dc.date.issued2025
dc.departmentTıp Fakültesi
dc.description.abstractThis study aimed to investigate the protective effects of carvacrol (CRV) on isoproterenol (ISO)-induced myocardial injury, focusing on its modulation of the Gal-3/TLR4/MYD88/NF-κB pathway. Thirty-five male Sprague Dawley rats were divided into five groups: control, CRV-treated, ISO-induced, and CRV pre-treated with two different doses (ISO + CRV 25 mg/kg and ISO + CRV 50 mg/kg). Cardiac markers, inflammatory cytokines, oxidative stress parameters, antioxidant enzymes, apoptosis, oxidative DNA damage, and endoplasmic reticulum (ER) stress were assessed. The study explored the impact of CRV on galectin-3 and the TLR4/MYD88/NF-κB pathway. ISO-induced myocardial injury was associated with elevated cardiac marker enzymes, inflammatory cytokines, oxidative stress, ERS, and activation of the Gal-3/TLR4/MYD88/NF-κB pathway. CRV treatment significantly attenuated these effects, showcasing its cardioprotective potential. Histopathological examination revealed reduced inflammatory cell infiltration with CRV pre-treatment. Furthermore, CRV significantly reduced oxidative stress parameters, including malondialdehyde (MDA) levels, and increased antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). The study highlighted the protective role of CRV against oxidative DNA damage, as indicated by decreased 8-OHdG levels. Additionally, CRV mitigated ERS by reducing ATF6 and GRP78 expression levels. It was also determined that CRV reduces apoptosis by regulating the expression levels of Bax (Bcl-2-associated X protein) and Bcl-2 (B-cell lymphoma 2), as well as AKT (Protein kinase B) protein levels. This comprehensive understanding underscores CRV's potential as a promising therapeutic agent for managing myocardial injury, providing valuable insights into its broader effects on cardiovascular health.
dc.identifier.doi10.1007/s44411-025-00315-1
dc.identifier.issn00069248
dc.identifier.scopus2-s2.0-105014273339
dc.identifier.scopusqualityQ2
dc.identifier.urihttps://doi.org/10.1007/s44411-025-00315-1
dc.identifier.urihttps://hdl.handle.net/20.500.12451/14491
dc.indekslendigikaynakScopus
dc.institutionauthorKandemir, Fatih Mehmet
dc.language.isoen
dc.publisherSpringer International Publishing
dc.relation.ispartofBratislava Medical Journal
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.titleInvestigating the effects of carvacrol in isoproterenol-induced myocardial injury: Role of H-FABP and Gal-3/TLR4/MYD88/NF-κB signaling pathway modulation
dc.typeArticle

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