Investigating the effects of carvacrol in isoproterenol-induced myocardial injury: 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, anti-oxidant enzymes, apoptosis, oxidative DNA damage, and endoplasmic reticulum stress (ERS) 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 ensured a significant reduction in oxidative stress parameters, including malondialdehyde (MDA) levels, and an increase in 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/GRP78 expression levels. It has also been determined that CRV reduces apoptosis by regulating the levels of Bax (Bcl-2-associated X protein) /Bcl-2 (B-cell lymphoma 2) expression levels and 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 effect on cardiovascular health.