The Protective Effect of Carvacrol Against Isoproterenol-Induced Cardiotoxicity in Rats

Isoproterenol (ISO)-induced myocardial injury involves oxidative stress (OS) and inflammation. Given carvacrol (CAR)'s antioxidant and cardioprotective properties, we aimed to investigate its protection against ISO-induced myocardial injury in rats.

Thirty male Wistar albino rats were assigned to three groups: Control; ISO (100 mg/kg, subcutaneous, for 2 days); and CAR+ISO (CAR 50 mg/kg/day, orally at 9:00, for 7 days + ISO at 16:00 on days 6-7). CAR and ISO doses were chosen based on prior evidence of CAR's antioxidant effects and ISO-induced oxidative cardiac stress. Diastolic and mean arterial pressures, corrected QT interval (QTc), T-wave changes, and serum troponin I levels were assessed. Cardiac OS biomarkers [malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT)] and histopathology were evaluated.

ISO markedly increased troponin I from 43.9 to 508.9 ng/mL and slightly reduced GSH from 1502.4 to 1330 nmol/g wet tissue and SOD from 1080.25 to 1010.34 U/g protein. ISO markedly reduced MDA (95.30 to 71.78 nmol/g wet tissue at 535 nm; 77.49 to 61.24 nmol/g wet tissue at 520 nm), likely due to depletion of lipid peroxidation substrates caused by excessive reactive oxygen species production, while slightly increasing CAT (132.66 to 162.04 K/g protein), possibly as a compensatory response. QTc and histopathological scores increased significantly; histopathological components were cardiomyocyte degeneration (CD) (range, 0.0 to 2.0), interstitial edema (IE) (range, 0.0 to 2.0), and granulation tissue (GT) (range, 0.0 to 1.0). CAR attenuated electrocardiographic abnormalities, significantly reduced troponin I (from 508.9 to 38.05 ng/mL), and restored GSH (from 1330 to 1396.8), SOD (from 1010.34 to 1094.42), and CAT (from 162.04 to 135.58). CAR significantly ameliorated histopathological scores: CD (2.0 to 1.0), IE (2.0 to 1.0), and GT (1.0 to 0.0).

CAR exerts protective effects against ISO-induced myocardial injury via antioxidant, membrane-stabilizing, and possible anti-arrhythmic properties. These findings support the therapeutic potential of CAR in OS-mediated cardiac pathologies and warrant further investigation in chronic and molecularly targeted models.