The level of hydrogen sulfide and morphological changes in the aorta of rats under the influence of vitamin D under the conditions of modulation of the H2S / cystathionine-γ-lyase system

Abstract

Annotation. Vitamin D and hydrogen sulfide (H2S) belong to pleitropic regulators, which are involved in the control of many cellular functions and biochemical processes, determine the adaptive potential of the cardiovascular system. The relationship between vitamin D and the H2S system is not fully investigated. The aim of the study was to evaluate the effect of the active form of vitamin D - calcitriol (1,25 (OH)2D3) on the morphological state of the thoracic aorta of rats and the level of it’s saturation with hydrogen sulfide under the conditions of the H2S / cystathionine-γ-lyase system modulation. The experiments were performed on 90 white male laboratory rats in accordance with the principles of bioethics (Strasbourg, 1986). 1,25(OH)2D3 was administered in doses of 0.1 μg/kg and 1 μg/kg for 4 weeks. Propargylglycine (50 mg/kg) and NaHS (1 mg/kg) were used to modulate the state of the H2S/cystathionine-γ-lyase system. The content of H2S was determined in the thoracic aorta and morphological changes were evaluated. Statistical calculations were performed in IBM Statistics SPSS 26, differences were evaluated in the Mann-Whitney test at the significance level of p<0.05. It was established that 1,25 (OH)2D3 in a dose of 1.0 μg/kg leads to the formation of H2S deficiency and a complex of morphological changes in the aorta, which are manifested by damage of epithelial cells and stromal elements, and the formation of calcifications. Modulation of the H2S / cystathionine-γ-lyase system is a factor that modifies the effect of high doses of 1,25 (OH)2D3 on vessels: H2S deficiency increases damage of the vascular wall, while increasing tissue H2S saturation has the opposite effect. 1,25 (OH)2D3 in a dose of 0.1 μg/kg shows the ability to increase the level of endogenous H2S and reduces the development of pathological changes in blood vessels under the conditions of long-term inhibition of the H2S / cystathionine-γ-lyase system.