Exploration of the Mechanism of Yangxinxue Decoction in Treating Myocardial Injury Based on Network Pharmacology and Molecular Docking

Background Coronary artery disease is a common cardiac ailment prevalent worldwide. Purpose To explore the therapeutic impacts and related mechanisms of Yangxinxue (YXX) granules on myocardial injury. Materials and Methods A mouse model of myocardial injury was induced, and different doses of YXX were used for intervention. The protective effects of YXX on mouse myocardium and related mechanisms were observed through pathological examination and Western blot. Network pharmacology methods were used to analyze the relevant mechanisms of YXX in treating unstable angina. Results Animal experiments showed that YXX significantly enhanced the serum superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels in isoproterenol (ISO)-treated mice, while reducing serum malondialdehyde (MDA), and alleviating the levels of cardiac troponin T in myocardial tissue after ISO treatment. YXX inhibited the elevation of vascular endothelial growth factor (VEGF) and hypoxia-inducible factor-1α (HIF-1α). The decrease of endothelial nitric oxide synthase (eNOS) in mouse myocardial tissue was caused by ISO but had no significant effect on the elevation of endothelin-1 (ET-1) and the decrease of phosphorylated Ser/Thr protein kinase B (p-AKT). YXX also inhibited the elevation of caspase-3 and caspase-9, as well as BAX expression, and the decrease of BCL-2 expression in mouse myocardial tissue after ISO intervention. Network pharmacology analysis identified 239 targets associated with the treatment of myocardial injury by YXX. Conclusion YXX can protect the myocardium, and its treatment of myocardial injury involves a complex mechanism with multiple targets and pathways, providing a new approach to the clinical treatment of unstable angina.