卷 20, 编号 2 (2022)

It is currently being discussed that the microbiota of the gastrointestinal tract and its metabolites affect the course of chronic heart failure (CHF). The purpose to summarize the available data on the role of the intestinal microbiota in the pathogenesis of CHF. Material and methods. A analysis of the main foreign and domestic sources on PubMed, MedLine, eLIBRARY databases over the last 20 years has been carried out. Results. In the course of the analysis of published works, the key links in the pathogenesis of CHF (imbalance of neurohumoral systems, inflammatory theory, metabolic disorders) and changes arising from disturbance of intestinal microbiota composition were compared. The results of studies where microbiota correction by prescribing antibiotics, probiotics and prebiotics resulted in positive effects on the course and prognosis in CHF are presented. Conclusion: Commonality in CHF pathogenesis (imbalance of neurohumoral systems, inflammatory theory and metabolic disorders) and changes in microbiota disturbances (including those mediated by microbial metabolites and inflammatory cytokines), the positive effects of pro- and prebiotics both on the microbial composition of the intestine and on course and prognosis in CHF, allow the consideration of microbiome as a marker and a possible target in CHF therapy. All of the above necessitates for further research in this area.

Introduction. The main reason for the severity of COVID-19 and the death of patients is the «cytokine storm» - a strong inflammatory response caused by SARS-CoV-2. Macrophages, immune cells that help eliminate pathogens and repair damaged tissues, play a key role in the expression of inflammatory mediators. In addition to known cytokines, macrophages express the PD-L1 protein, a ligand of the PD1 apoptosis receptor. The aim of the study was to comparatively analyze the levels of soluble forms of the programmed cell death receptor (sPD-1) and its ligand (sPD-L1), as well as biochemical and hematological parameters in the blood of patients who underwent COVID-19. Material and methods. We carried out sPD-1 and sPD-L1 enzyme immunoassay and biochemical studies in 72 employees of the N.N. Blokhin National Medical Research Center of Oncology of the Ministry of Health of the Russian Federation who have undergone COVID-19. The control group consisted of 57 healthy donors. The fact of the disease was confirmed by the presence of antibodies to class G immunoglobulins (SARS-Cov-2 IgG) in the blood serum using the ELISA test system Antigma-G (Generium, Russia). The concentrations of sPD-1 and sPD-L1 in blood serum were studied using the Human sPD-L1 ELISA kit and Human sPD-1 ELISA kit (Affimetrix, eBioscience, USA). The levels of iron, transferrin and ferritin were determined on an automatic analyzer Cobas (Roche). Complete blood count was performed on an automatic Sysmex XE-2100 analyzer (Japan). Results. In the serum of those who underwent COVID-19 (30-50 days after the onset of the first symptoms), there was a significant decrease in sPD-L1 levels and a change in the correlation between the components of the sPD-1 / sPD-L1 system. A statistically significant direct relationship was found between the concentrations of soluble forms of the sPD-1 receptor and its ligand sPD-L1 with the levels of iron, hemoglobin and the number of erythrocytes, as well as between sPD-L1 and ferritin. No relationship was found between sPD-1 and sPD-L1 levels and erythrocyte counts (MCV, MCH, RDW-SD). Conclusion. The results obtained expand the understanding of the role of sPD-1 and sPD-L1 in persons who have undergone COVID-19, demonstrate the relationship between the processes of apoptosis, some biochemical and hematological parameters of blood serum, and are the basis for further research.

Introduction. The study of intermoleculars interactions can contribute to the development of ideas about the violation of the endothelium,s adhesive function as one of the pathogenetic links in the development of peripheral artery diseases of atherosclerotic etiology. The aim of the study. To study the content of P- and E-selectins, a high-affinity glycoprotein ligand PSGL-1; to identify correlations between the represented values in the blood serum of patients with atherosclerosis of the lower extremities arteries. Methods. Quantitative determination of selectins P., E and glycoprotein ligand PSGL-1 by the sandwich method of ELISA in blood serum. Results. A decrease in the concentrations of selectins P and E, an increase in the concentration of the glycoprotein ligand of selectins PSGL-1 was revealed; a moderate negative correlation (r = -0,48) between the concentration of selectin P and the concentration of PSGL-1 in the blood serum of patients with atherosclerosis of the arteries of the lower extremities was detected. The findings of the study are as follows: • a statistically significant decrease in the concentration of selectin P in the blood serum of patients with atherosclerosis of the arteries of the lower extremities was revealed; • a statistically insignificant decrease in the concentration of selectin E in the blood serum of patients with atherosclerosis of the arteries of the lower extremities was detected; • a statistically significant increase in the concentration of glycoprotein ligand selectins PSGL-1 in the blood serum of patients with atherosclerosis of the arteries of the lower extremities was detected; • a moderate negative relationship was found between the concentration of selectin P and PSGL-1 (r = -0.48) in the blood serum of patients with atherosclerosis of the arteries of the lower extremities. All of the above changes can be related to the death of endotheliocytes and their reduction in synthesis of intercellular adhesion molecules, which is reflected in the disruption of the adhesive function, which is a component of endothelial dysfunction.

Introduction. Currently, understanding the molecular mechanisms of pathological angiogenesis remains a fundamental problem in hepatology. The aim of this work was to find a relationship between the level of mRNA expression of the ang, vegf genes and angiogenesis in the liver of Wistar rats in experimental cirrhosis. Methods. The experiment used 117 sexually mature male Wistar rats weighing from 190-210g. Liver cirrhosis in animals was induced with a solution of thioacetamide, which was introduced into the stomach using a probe at a dose of 200 mg/kg of animal body weight 2 times a week. The dynamics of the process was studied at nine time points (over 17 weeks). The level of mRNA expression of the ang and vegf genes in the liver was studied by real-time polymerase chain reaction. To obtain overview histological preparations, liver sections were stained with hematoxylin and eosin, and to identify connective tissue - by the Mallory method. Microscopic analysis was performed using an OLYMPUS BX51 microscope and ImageScope Color and cellSens Standard image analysis programs. The degree offlbrosis was assessed using the Ishak K.G. Conclusion. A statistically significant relationship was established between the level of expression of the total mRNA of target genes, angiogenesis of the venous system, and fibrogenesis. No pronounced morphological changes were observed on the part of the liver arterial system throughout the experiment; arterial angiogenesis was not identified. Probably, the spliced forms of mRNA of the ang and vegf genes estimated by us are more important factors in the pathological angiogenesis of the venous system. Significant correlations were found between target genes r=0.65-0.84 (splice variants that were investigated). The joint study of genes with respect to each other is a necessary additional parameter when conducting basic and preclinical research.