Akademik Veri Yönetim Sistemi
Bratislava Medical Journal, 2025 (SCI-Expanded)
Aim: Diclofenac (Diclo) is a widely used nonsteroidal anti-inflammatory drug (NSAID) for managing pain, inflammation, and joint disorders. However, studies have shown that diclofenac may induce cardiotoxicity via oxidative stress, inflammation, apoptosis, ER stress, and autophagy. Carvacrol (CRV), a natural monoterpenoid phenol, exhibits antioxidant, anti-inflammatory, and cytoprotective properties. This study aimed to evaluate the protective effects of carvacrol against diclofenac-induced cardiotoxicity by assessing relevant molecular and histological markers. Methods: In the study, 35 Wistar rats were divided into 5 groups; Control, CRV, Diclo, Diclo + CRV25, and Diclo + CRV50. Diclo was administered intraperitoneally at a dose of 50 mg/kg. CRV (25 mg/kg and 50 mg/kg) was administered via oral gavage. Biochemical, molecular, and histological methods were used to investigate indicators of oxidative stress, inflammation, apoptosis, and ER stress damage in heart tissue. Results: CRV treatment attenuated oxidative stress damage by reversing Diclo-induced changes: it significantly increased the levels of antioxidant markers (SOD, CAT, GPx, GSH) and decreased MDA levels, a marker of lipid peroxidation. CRV also reduced inflammatory mediators such as NF-κB and other pro-inflammatory cytokines. Furthermore, CRV downregulated apoptotic markers Bax and Caspase-3 while upregulating anti-apoptotic markers AKT-2 and Bcl-2. ER stress-associated proteins (ATF-6, PERK, IRE1, GRP-78) elevated by Diclo were also reduced by CRV. In addition, CRV alleviated structural and functional cardiac damage induced by Diclo. Conclusion: Overall, CRV may be an effective treatment option for cardiac tissue damage caused by Diclo toxicity and may reduce the level of damage.