The influence of calcitriol on indicators of apoptosis, inflammation and oxidative stress in the myocardium of rats under conditions of modulation of the hydrogen sulfide / cystathionine-gamma-lyase system

Abstract

Annotation. Vitamin D plays an important role in the control of the cardiovascular system, including myocardial remodeling and hypertrophy. Hydrogen sulfide (H2S) is an important mediator of cardiomyocyte adaptive mechanisms to stress factors. The role of the H2S system in the mechanisms of biological action of vitamin D in the cardiovascular system has not been clarified. The aim of the work was to determine the effect of the active form of vitamin D - calcitriol on the indicators of apoptosis, inflammation and oxidative stress in the myocardium of rats under conditions of modulation of the H2S / cystathionine-γ-lyase system. The experiments were performed on 90 white male laboratory rats in accordance with the principles of bioethics (Strasbourg, 1986). Over a period of 4 weeks, 6 groups of animals were administered 1,25 (OH)2D3 at doses of 0.1 and 1 μg/kg. To modulate the H2S system, propargylglycine (PPG) and NaHS were administered. The H2S content, markers of inflammation, apoptosis, and oxidative stress were determined in the myocardium. Statistical analysis was performed using the IBM Statistics SPSS 26 software package. It was established that 1,25 (OH)2D3 in a dose of 0.1 μg/kg increases the level of H2S in the myocardium, while at a dose of 1 μg/kg it has an inhibitory effect on the H2S system. Modulators of H2S exchange modify pathochemical changes in the myocardium induced by 1,25 (OH)2D3 at a dose of 1 μg/kg. PPG potentiates the increase in the levels of mediators of inflammation and apoptosis, deepens the imbalance in the system of heat shock proteins and signs of oxidative stress. Administration of NaHS does not cause significant changes in myocardial parameters under the influence of a physiological dose of 1.25 (OH)2D3 and significantly reduces the pro-apoptotic and pro-inflammatory effects of a high dose of 1.25 (OH)2D3.