Mulberroside A Alleviates Myocardial Infarction by Inhibiting Oxidative Stress and Apoptosis Via the PI3K/Akt Signaling Pathway

Myocardial infarction (MI), a coronary-related condition that poses a significant threat to life, featured by the occurrence of sudden cardiac death. Cortex Mori radices extract can attenuate myocardial injury in diabetic rats. The study aimed to explore the role of mulberroside A (MBA), a component from Cortex Mori, in isoproterenol (ISO)-induced mouse model of MI. Hematoxylin–eosin (H&E) staining of mouse cardiac tissues was performed to measure pathological changes in context of ISO and/or MBA treatment. Serum levels of lactate dehydrogenase (LDH) and brain natriuretic peptide (BNP) were assessed to examine myocardium damage. Transthoracic echocardiography was used to analyze ejection fraction (EF) and fractional shortening (FS). Expression levels of fibrotic markers were measured by RT-qPCR and western blotting. Serum levels of cardiac function indicator (creatine kinase) and oxidative stress markers were measured using corresponding kit. Protein levels of apoptotic markers and factors associated with the PI3K/Akt signaling were measured by western blotting. MBA alleviated ISO-induced cardiac damage and lowered high expression levels of cardiac fibrosis indicators in the mouse model of MI. MBA significantly improved ISO-induced cardiac dysfunction in mice. Additionally, the inactivation of the p-PI3K and p-Akt signaling induced by ISO was rescued by MBA administration. The inhibition of the PI3K/Akt signaling using LY294002 counteracted the anti-apoptotic and anti-oxidative effects mediated by MBA in MI mouse model. MBA ameliorates ISO-induced myocardial injury by suppressing cardiomyocyte apoptosis and improving oxidative injury via activation of the PI3K/Akt signaling.