The protective role of bFGF in myocardial infarction and hypoxia cardiomyocytes by reducing oxidative stress via Nrf2.

Myocardial infarction (MI) remains a major health-related problem with high incidence and mortality rates. Oxidative stress plays an important role in myocardial ischemia injury and further leads to myocardial remodeling. Basic fibroblast growth factor (bFGF) is a member of the fibroblast growth factors that regulate a variety of biological functions. However the function of bFGF in myocardial infarction is still unknown. Here we aimed to investigate the role of bFGF and its underlying mechanism in ischemia heart and cardiomyocytes apoptosis. We found that bFGF treatment could significantly enhance the cardioprotective effects by reducing oxidative stress both in vivo and vitro. In addition, we found that bFGF activated Nrf2-mediated antioxidant defenses via Akt/GSK3β/Fyn pathway. Furthermore, Nrf2 knockdown largely counteracted the protective effect of bFGF. In summary, our study suggested that bFGF could alleviate myocardial infarction injury and cardiomyocytes apoptosis via Nrf2.