Influence of androgen on myocardial apoptosis and expression of myocardial IR and IRS‑1 in chronic heart failure rat models.

The present study aimed to investigate the effect of androgens on chronic heart failure (CHF) in a rat model. A total of 120 Sprague Dawley male rats were randomly divided into the following groups: (A) sham operation group, (B) castrated group, (C) heart failure (HF) group, (D) castrated + HF group, and (E) castrated + HF + testosterone (T) replacement therapy group. There were 20 rats in group A, and 25 rats in the other groups. Surgical castration was performed on groups B, D and E, and T replacement therapy was administered to group E. Groups C, D and E were treated with doxorubicin hydrochloride to prepare the CHF animal model. The insulin sensitivity index (ISI) was calculated from fasting blood glucose and fasting insulin levels. Echocardiography was performed. Venous blood was collected for plasma T level test. Myocardial tissue was used for apoptosis index analysis. The expression levels of myocardial insulin receptor (IR) and insulin receptor substrate‑1 (IRS‑1) were measured by reverse transcription semi‑quantitative polymerase chain reaction. Compared with group A, the T level and ISI decreased, whereas the expression level of IR and IRS‑1 were increased in the CHF group (P<0.05). Following castration, the T level and ISI were significantly decreased, and the expression of IR and IRS‑1 were increased compared with the uncastrated CHF rats (P<0.01). Following androgen administration, the ISI increased, expression of IR and IRS‑1 decreased, and the myocardial apoptosis index decreased (P<0.05). Taken together, these results demonstrated that androgen supplementation could improve insulin resistance and affect the expression of IR and IRS‑1 in CHF, thereby reducing myocardial apoptosis and improving cardiac function.