Abstract
The purpose of this study was to clarify the protective role of mangiferin on postinfarction myocardial remodeling and potential mechanisms. The myocardial infarction (MI) model was established by ligating the left anterior descending coronary artery. Cardiac function, myocardial apoptosis and fibrosis, serum tumor necrosis factor-α (TNF-α) and phosphorylated p38 mitogen-activated protein kinase (MAPK) were examined by echocardiography, histological staining, ELISA and Western blot, respectively. Mangiferin attenuated MI and prevented the development of intercellular fibrosis. Western blotting underscores that the p38 MAPK cascade plays an important role in the cardioprotective effect of mangiferin during MI. Inhibition of p38 MAPK significantly decreased serum TNF-α levels. Transferase-mediated uridine nick end labeling and Masson staining also showed that mangiferin reduced apoptosis and fibrosis in myocardium remodeling. Based on these results, we conclude that mangiferin has a therapeutic effect on post-MI left ventricular remodeling and improves cardiac function.
Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
