Mechanism of Buyang Huanwu Decoction in Improving Heart Failure after Myocardial Infarction by Inhibiting Platelet Aggregation via Platelet Glycoprotein VI: An Investigation Based on Molecular Docking and Surface Plasmon Resonance

Abstract Objective: Postmyocardial infarction heart failure (HF post-MI) induces platelet disorders, increased blood viscosity, and thrombosis. Buyang Huanwu decoction (BHD), a classical Chinese formulation for Qi deficiency and blood stasis, has proven clinical efficacy. However, its pharmacodynamic basis remains unclear. Platelet glycoprotein VI (GPVI) plays a crucial role in collagen-induced activation and aggregation of platelets. In this study, focusing on GPVI and its downstream signaling pathways, the potential pharmacodynamic material basis of BHD’s therapeutic effects in rats with postmyocardial infarction heart failure was investigated. Materials and Methods: Rat models of myocardial infarction-induced heart failure were established by left anterior descending artery ligation, treated with BHD (6 g/kg, 13 g/kg) or aspirin for 14 days, alongside normal and model groups. Results: BHD significantly improved cardiac function in HF post-MI rats, as shown by serology, echocardiography, and histopathology. In addition, BHD alleviated blood stasis and thrombosis by reducing platelet activation/aggregation. BHD also modulated the expression levels of platelet GPVI and its downstream target proteins through Western blotting, molecular docking, and surface plasmon resonance assays. The active components of BHD, peoniflorin, astragaloside A, and calycosin-7-O-β-D-glucoside, showed good binding affinity to GPVI. Conclusions: BHD protected cardiac function by inhibiting platelet aggregation, which may be associated with the strong binding affinity of the active components to GPVI, thereby inhibiting the expression of GPVI and its downstream signaling proteins.