Influence of dysbiotic syndrome on the formation of experimental nepropathy

Abstract

Kidneys are sensitive to damage by pathogenic factors of dysbiotic syndrome, among which lipopolysaccharide is the main one. However, the influence of the dysbiotic syndrome on the formation of nephropathy has not been studied enough.

The aim of the study is to determine the effect on the kidneys of rats of an experimental dysbiotic syndrome, which was modeled using the antibiotic lincomycin in combination with the administration of epinephrine.

Material and methods. Experimental dysbiotic syndrome (systemic dysbiosis) was reproduced in 21 Wistar rats (female, 11 months old, average weight 310±25 g) by administration of lincomycin with adrenaline hydrotartrate. The activity of urease and lysozyme was determined in blood serum and tissue homogenates and the degree of dysbiosis was calculated. The condition of the kidneys was assessed by the activity of elastase, urease, lysozyme, catalase, the content of malondialdehyde (MDA), creatinine, indicators of antioxidant protection.

Results. The level of urease increases in the liver of rats with experimental dysbiosis by 2.3 times, in the mucous membrane of the stomach - by two times, and in blood serum - by 2.3 times. The activity of lysozyme decreases in rats with dysbiosis: in the liver - by 42%, in the stomach - by 36%, and in blood serum - by 32%. Urease activity in the kidneys increases by 76%, lysozyme activity decreases by 33%, which indicates a 2.6-fold increase in the degree of dysbiosis. As a result of dysbiosis in the kidneys, the level of biochemical markers of inflammation significantly increases: elastase by 79.5% and MDA by 18%, catalase activity significantly decreases (by 6%).

Conclusions. The combined administration of lincomycin and adrenaline causes the development of a dysbiotic syndrome in experimental animals. Under the condition of modeling the dysbiotic syndrome, an inflammatory-dystrophic process develops in the kidneys, and the level of antioxidant protection significantly decreases. Under conditions of experimental dysbiosis, pathological processes in the kidneys are manifested to a lesser extent than in other organs, possibly due to the high initial level of lysozyme in the tissue.