The effects of apocynin on ciprofloxacin-induced oxidative stress-related cardiotoxicity

Ciprofloxacin (CFX), a fluoroquinolone antibiotic, is known to induce oxidative stress–mediated cardiotoxicity. This study investigates the potential protective and therapeutic effects of apocynin (APO), a selective NADPH oxidase (NOX) inhibitor and potent antioxidant, against CFX-induced myocardial injury in rats. Thirty-two male Wistar albino rats were randomly divided into four groups (n = 8). CFX (25 mg/kg, i.p.) was administered twice daily for one week, while APO (20 mg/kg, i.p.) was given once daily for four days either before or after CFX treatment. Hemodynamic parameters (heart rate, systolic, diastolic, and mean blood pressures) and electrocardiographic (ECG) indices (PR, QRS, and QT intervals) were recorded invasively. Histopathological evaluations assessed myocardial inflammation, cardiomyocyte degeneration, and aortic intima–media thickness. Biochemical analyses of cardiac and aortic tissues included measurements of malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) levels. CFX administration significantly elevated cardiac MDA by ~ 45% and decreased SOD and CAT activities by ~ 30–35% (p < 0.05) compared with controls. These alterations were markedly attenuated in APO-treated rats, where antioxidant enzyme activities increased by ~ 25–40% and MDA levels were restored toward normal values (p < 0.05 vs. CFX). APO also shortened the QT interval by ~ 15% and improved systolic pressure by ~ 12% compared with the CFX group (p < 0.05). Histopathological findings confirmed reduced myocardial degeneration and inflammatory infiltration in both APO + CFX and CFX + APO groups. APO effectively ameliorated CFX-induced cardiac oxidative injury by inhibiting NOX2-mediated reactive oxygen species formation and restoring antioxidant defense mechanisms, leading to functional improvement in ECG and hemodynamic parameters. These results suggest that targeted NOX inhibition may represent a practical pharmacological approach to reduce fluoroquinolone-associated cardiotoxicity, warranting further translational investigation.