Myocardial remodeling is one of the important pathological basis when myocardial infarction or pressure overload occurs, whereas mangiferin which is a naturally occurring xanthone has a broad range of therapeutic effect on postinfarction myocardial remodeling. Mangiferin attenuates myocardial infarction by preventing the accumulation of myocardial collagen and the development of intercellular fibrosis. Mangiferin's inhibition to p38 mitogen activated protein kinases plays an important role in the cardioprotective effect. Inhibition of p38 mitogen activated protein kinases significantly decreases TNF-α and then brings the cardioprotective effect. Similarly, p38 mitogen activated protein kinases in pressure overload disease also play a very important role. Understanding of these has direct implications for clinical therapy.
ObjectiveTo establish a mouse model of pressure overload-induced heart failure via suprasternal notch approach. MethodsMale mice were separated into a sham group and an experiment group. Through suprasternal notch approach, the aortic arch port between the origin of the right innominate and left common carotid arteries was partially clipped with tantalum clip, which had a remaining opening of 0.35 mm or 0.25 mm in diameter to cause progres-sively increased afterload. Echocardiography was performed 10 weeks after aortic arch clipped or sham surgery to deter-mine left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), left ventricular posterior wall end-diastolic thickness (LVPWD), ejection fraction (EF) and fractional shortening (FS). After hemodynamic recordings were completed, mouse body weight (BW) and heart weight (HW) were measured for obtaining HW/BW ratio (mg/g). After heart function examination, mice blood sample was collected for evaluation of serum N-terminal pro-brain natriuretic peptide (NT-proBNP). At the end, part of left ventricular free wall was excised, and hematoxylin and eosin stain was made for histopathological examination. ResultsThe HW/BW, LVEDD and serum NT-proBNP significantly increased in the experiment group compared with those in the sham group (P < 0.01, respectively). The LVPWD, EF and FS significantly decreased compared with the sham group (P < 0.01, respectively). Histopathological examination showed malalignment and rupture of cardiac muscle fibers, hypertrophy and degeneration of myocardial cells, part of which had local or patchy necrosis in left ventricule postoperatively 10 weeks. ConclusionThe model of pressure overload-induced heart failure in mice established through suprasternal approach is simple, minimally invasive and reliable.