Testosterone suppresses ventricular remodeling and improves left ventricular function in rats following myocardial infarction

Author：

Publisher： Spandidos Publications

E-ISSN： 1792-1015|9|4|1283-1291

ISSN： 1792-0981

Source： Experimental and Therapeutic Medicine, Vol.9, Iss.4, 2015-01, pp. : 1283-1291

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Abstract

Men with congestive heart failure (CHF) have relatively low testosterone levels. Several studies demonstrated that testosterone treatment increases cardiac output and reduces peripheral vascular resistance. However, the effects of testosterone on heart function, cardiomyocyte apoptosis and ventricular remodeling have not been fully elucidated. This study was conducted to investigate the effects of testosterone on heart function, cardiomyocyte apoptosis and ventricular remodeling in male rats postmyocardial infarction. A total of 86 male rats were randomly assigned to undergo ligation of the coronary artery (n=70) or pseudosurgery (n=16). After 6 weeks, a left ventricular ejection fraction (LVEF) of ≤45% was defined as a successful model of CHF. the model rats were randomly assigned to 3 groups, namely lowdose testosterone (TU), highdose TU and placebo (PL) groups. After treatment for 12 weeks, the expression of several mRNA transcripts in myocardial tissue was measured by quantitative polymerase chain reaction. Immunofluorescence was used to measure myocardial caspase3 expression. Compared to the PL group, LVEF was significantly improved in the TU treatment groups. Moreover, the mRNA expression of atrial natriuretic peptide, brain natriuretic peptide, matrix metalloproteinase2 and sarcoendoplasmic reticulum Ca2+ATPase 2a was significantly reduced, while the mRNA expression of glycogen synthase kinase 3β and tissue inhibitor of metalloproteinase2 was markedly increased in the TU groups. TU treatment also significantly reduced caspase3 expression. Therefore, different doses of TU suppressed ventricular remodeling and improved left ventricular function, reduced apoptosis and prevented mortality in a CHF rat model.