Investigating the Effects of Carvacrol in İsoproterenol-İnduced Myocardial İnjury: Role of H-FABP and Gal-3/TLR4/MYD88/NF-κB Signaling Pathway Modulation

This 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.