Biochanin A Mitigates Oxidative Stress and Inflammation in Diabetic Myocardial Infarction: Insights From a Streptozotocin and Isoproterenol Rat Model

This study evaluates the cardioprotective potential of biochanin A (BCA), a naturally occurring isoflavonoid with antioxidant and anti-inflammatory properties, in a streptozotocin (STZ) and isoproterenol (ISO)-induced model of diabetic myocardial infarction (DMI) in rats. Male Wistar rats were divided into five groups, including normal controls, STZ+ISO, and three BCA-treated groups (5, 10, and 20 mg/kg). Results: BCA administration significantly improved electrocardiographic parameters by reducing ST height and QT interval prolongation (p < 0.05). It also reduced myocardial injury markers (lactate dehydrogenase (LDH), creatinine kinase on myocardial bundle (CK-MB), aspartate transaminase (AST), and cardiac troponin-T (cTn-T)) in a dose-dependent manner (p < 0.001). BCA normalized blood pressure, heart rate, and left ventricular function, improving maximum and minimum rate of ventricular contraction (+dP/dt, -dP/dt) (p < 0.01). Furthermore, BCA significantly decreased blood glucose levels and improved lipid profiles by lowering total cholesterol (TC), triglycerides (TG), and low-density lipoprotein (LDL) while increasing high-density lipoprotein (HDL) levels (p < 0.001). It suppressed inflammation by reducing tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β levels (p < 0.01). Oxidative stress markers, including malondialdehyde (MDA), were reduced, while antioxidant markers such as glutathione (GSH), superoxide dismutase (SOD), and catalase were increased (p < 0.001). BCA enhanced nuclear factor erythroid 2-related factor 2 (Nrf2) expression, promoting antioxidant defense. Histopathological analysis confirmed reduced myocardial injury and improved cardiac architecture. Conclusion: These findings highlight BCA's potential as a therapeutic agent for managing DMI through its dual antioxidant and anti-inflammatory actions.