Abstract:

BACKGROUND: Hepatocyte growth factor is a kind of myocardial nutritional factors. It has a strong inhibitory effect on myocardial apoptosis and ventricular remodeling. Meanwhile, it promotes the mitosis of vascular endothelial cells.
OBJECTIVE: To explore the protective effect of hepatocyte growth factor on model mice of acute decompensated heart failure.
METHODS: A total of 50 Kunming mice were randomly divided into five groups: normal control group, chronic heart failure group, acute decompensated heart failure group, chronic heart failure treated group and acute decompensated heart failure treated group. Chronic heart failure model in mice was constructed using tail intravenous injection of adriamycin. Mice in the corresponding group were intravenously injected with bacterial lipopolysaccharide through tail vein to construct acute decompensated heart failure model. Mice in the chronic heart failure treated group and acute decompensated heart failure treated group were intravenously injected with hepatocyte growth factor through tail vein.  
RESULTS AND CONCLUSION:Compared with chronic heart failure group, the thickness of ventricles and left ventricular ejection fraction in the chronic heart failure treated group increased significantly; the content of interleukin-6 and brain natriuretic peptide decreased; the expression of Bax protein decreased while the expression of Bcl-2 protein increased; the myocardial apoptosis reduced significantly (  < 0.01 or  < 0.05). Compared with acute decompensated heart failure group, the thickness of ventricles P P and left ventricular ejection fraction in the acute decompensated heart failure treated group increased significantly; the content of brain natriuretic peptide decreased while the content of interleukin-6 decreased significantly; the expression of Bax protein decreased while the expression of Bcl-2 protein increased (  < 0.01 or   < 0.05). These findings indicate that hepatocyte growth P Pfactor significantly improve the heart function of acute decompensated heart failure mice by anti-inflammatory effect and resisting cardiac muscle cell apoptosis.