Evaluation of vinpocetine in an acute doxorubicin-induced cardiotoxicity model in rats.

Doxorubicin (DOX) is an effective antineoplastic agent whose clinical use is limited by cardiotoxicity. This study aimed to evaluate the potential protective effects of vinpocetine (VINPO) in an acute DOX-induced cardiotoxicity model in rats. Thirty-two male Wistar albino rats were randomly assigned to four groups: Control, DOX (20 mg/kg, single intraperitoneal dose), VINPO (10 mg/kg for 3 days), and VINPO + DOX. Forty-eight hours after DOX administration, electrocardiography (ECG), heart rate (HR), blood pressure (BP), and oxygen saturation were recorded. Serum troponin-I, creatin kinase (CK), and CK-MB mass levels were measured. Myocardial and vascular tissues were analyzed for malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and reduced glutathione (GSH). Histopathological and caspase-3 immunohistochemical evaluations were also performed. DOX administration resulted in significant alterations in vascular antioxidant enzyme activities and increased myocardial histopathological injury scores compared with controls. VINPO partially modulated certain oxidative stress parameters, particularly vascular SOD and CAT activities. However, serum cardiac biomarkers, ECG parameters, and caspase-3 immunoreactivity did not differ significantly among groups. Histopathological myocardial injury was not significantly improved in the VINPO + DOX group compared with DOX alone. VINPO demonstrated modest modulatory effects on selected oxidative stress parameters in acute DOX-induced cardiotoxicity. However, these effects were not consistently supported by functional or histopathological findings. Further studies using more severe or longer-term cardiotoxicity models are warranted to clarify its cardioprotective potential.