Cardioprotective effects of Amygdalin, a promising antioxidant, on acute myocardial infarction and underlying mechanisms

Abstract

Amygdalin (Amy) is a cyanogenic glycoside that mainly exists in the seeds of Rosaceae family members, such as peaches, apricots, and bitter almonds. The pharmacological effects of Amy on acute myocardial infarction (AMI) have not been explored yet. Hence, this study aims to explore the potential antioxidant activity of Amy in AMI and its underlying mechanisms. Bioinformatics analysis showed that Amy had a promising antioxidant activity in AMI through mitogen-activated protein kinase (MAPK) and AKT-related signaling pathways. Four proteins, superoxide dismutase 2 (SOD2), nuclear factor erythroid-2-related factor 2 (Nrf2), AKT1, and p38, were identified as potential targets of Amy against AMI damage based on the constructed protein–protein interaction network. Molecular docking revealed the potential binding sites between Amy and target proteins, and molecular dynamics simulations further confirmed the results. In vitro and in vivo experiments revealed that Amy significantly reduced reactive oxygen species production while enhancing the activity of antioxidant enzymes and attenuating cardiomyocyte apoptosis as well as cardiac dysfunction, partly through MAPK- and AKT- related signaling pathways.

Keywords

• Ischemic heart disease
• Oxidative stress
• Computational pharmacology
• MAPK and AKT signaling pathway