CASPASE-3 ACTIVITY IN CARDIAC TISSUE UNDER LONG-TERM RELEASING HORMONE BLOCKADE AND QUERCETIN ADMINISTRATION IN MALE RATS

Introduction. Caspase-3 is a key enzyme in apoptosis, though its exact role in programmed cell death remains incompletely understood. Studies have demonstrated that caspase-3 plays a critical role in cell death in specific cell types or under particular stimuli, as well as in initiating and completing biochemical processes associated with apoptosis. Men with congestive heart failure often exhibit reduced testosterone levels, and research suggests that testosterone therapy can improve cardiac output and lower peripheral vascular resistance. However, its effects on cardiac function, cardiomyocyte apoptosis, and ventricular remodeling remain unclear. The aim of this study was to examine the impact of testosterone suppression on caspase-3 activity in cardiac tissues during long-term releasing hormone blockade in male rats treated with quercetin. Materials and methods. The study was conducted on 60 sexually mature male rats. The animals were randomly divided into two groups: control (n=10) and experimental (n=50). In order to modulate central deprivation of luteinising hormone synthesis, animals in the experimental group received solution of tryptorelin at a dose of 0.3 mg of active ingredient per kg of body weight and quercetin at 100 mg/kg of body weight 3 times a week. Results. Immunohistochemical analysis of caspase-3 showed that caspase 3 increased sharply to a maximum on the 30th day of observation after the administration of tryptorelin, followed by a gradual significant decrease in this indicator on the 180th and 365th days at p˂0.05. When tryptorelin and quercetin were administered, as shown in Fig. 2, the main pattern (a sharp increase on day 30 and then a gradual decline until day 365) is preserved, but the reliability of the decrease in the quantitative parameter is significant only on days 30 and 90 of the study. Conclusions. The addition of quercetin to the diet leads to a decrease in the immunoreactivity of heart cells in experimental animals by caspase-3 expression, which can be regarded as a compensatory phenomenon aimed at balancing apoptosis in the conditions of hormonal dysfunction by suppressing testosterone synthesis.