HF model was established by abdominal aorta constriction in rats and incubation with 50 μM isoproterenol for 48 h in H9C2 cells. Various molecular biological experiments were performed to assess the effects of baicalein on cardiac function, myocardial remodeling, apoptosis and Ca2 + handling proteins.
In the present study, first we found that baicalein alleviated HF in vivo. Additionally, treatment with baicalein inhibited the myocardial fibrosis, restrained the expression and activity of MMP2 and MMP9, and suppressed apoptosis in heart tissue. Moreover, baicalein could inhibit the cardiac myocyte hypertrophy and apoptosis induced by isoproterenol in vitro. Finally we found that baicalein could modulate the expressions and activities of Ca2 + handling proteins, including downregulation of phosphorylation of Ca2 +/calmodulin-dependent protein kinase II (CaMKII) and expression of Na(+)/Ca(2 +)-exchangers (NCX1), upregulation of sarcoplasmic reticulum Ca(2 +) ATPase 2 (SERCA2) and ryanodine receptor 2 (RYR2). Baicalein also restrained the decreased SERCA activity induced by aortic banding.
Our studies suggested that baicalein alleviated myocardial remodeling and improved cardiac function via modulation of Ca2 + handling proteins, which may be a potential phytochemical flavonoid for therapeutics of HF.