Abstract
The aim of the study was to study the structural changes of the intestinal epithelial barrier in the duodenum in burn injury of skin in rat under experimental streptozotocin-induced diabetes mellitus. The study was carried out on laboratory white adult rats-males weighing 180-210 g. The control group consisted of 21 animals without somatic pathology, the first experimental group was 21 rats with burn skin injury, the second experimental group was 21 rats with burn skin and experimental streptozotocin-induced diabetes mellitus. The experimental diabetes model was reproduced by administering streptozotocin to the rats intraperitoneally at a single dose of 50 mg/kg. Thermal burn skin damage in rats corresponded to II – A-B degrees of dermal surface burn (according to the old classification III – A degree) with a total area of 21-23 % of the body surface with the development of burn shock. Duodenum was selected for morphological studies, fragments of which were processed by conventional methods of light and electron microscopy. The main criteria for assessing damage to the duodenal mucosa enterocytes were the results of a study comparing histological and ultrastructural data in dynamics at 7, 14, and 21 days after skin burns. The results of the studies showed that the base of damage to the intestinal epithelial barrier of the duodenum are deep destructive changes, which after 21 days (in the stage of septicotoxemia), as a rule, are not reverse and develop on the background of significant intoxication of the body. There was a decrease in the number of tight junctions in the intestinal epithelial barrier of the duodenum of rats of the first and second experimental groups and a loss of ordering (acquisition of some chaotic nature) of their localization as the time after burn injury increased. For the most part, the intestinal epithelial barrier loses the integrity of the cellular component with partial preservation of the basement membrane (the first occurs both due to necrosis of the enterocytes with a brush border and due to complete destruction of goblet cells). In all cases, defects exist in the intestinal epithelial barrier, which are potential pathways for paracellular translocation of the pathogenic contents of the duodenum. It is not inconceivable that part of this intestinal pathogenic content can be translocated also by partially damaged cells. Evidence of the latter is the presence of microbial bodies in the cytoplasm of cells with partially destroyed plasmalemma (but preserved organelles and nucleus). An adaptive mechanism for ensuring the repair of damaged enterocytes is selective autophagy, which acts as a factor in the recycling of destroyed organelles and the cytoplasmic matrix, aimed primarily at maintaining cell viability.
Highlights
Nowadays, due to the acceleration of urbanization and the growth of industrial use of heat energy, severe thermal burn injury resulting in burn disease is becoming one of the most important problems of practical medicine [26]
An adaptive mechanism for ensuring the repair of damaged enterocytes is selective autophagy, which acts as a factor in the recycling of destroyed organelles and the cytoplasmic matrix, aimed primarily at maintaining cell viability
In enterocytes of the mucous membrane of the duodenum of animals of the first experimental group 7 days after burns, the most characteristic feature of structural changes is the destruction of microvilli of the brush border of enterocytes, as well as changes of tight junctions
Summary
Due to the acceleration of urbanization and the growth of industrial use of heat energy, severe thermal burn injury resulting in burn disease is becoming one of the most important problems of practical medicine [26]. The ancient theory that autonomic neuropathy is a major contributor to diabetic enteropathy [17, 18, 25] has recently been supplemented by new theories of disease development [2]. It is believed [11] that hyperglycemia and its associated oxidative stress in neural networks, including nitrergic neurons and interstitial cells of Cajal [2, 23], play a central role in the development of diabetic enteropathy. The authors of the latest (at the time of publication) scientific review article "Diabets and the small intestine" [11] indicate that the latest scientific results are promising, but there is still a great need for further studies of the pathogenesis of diabetic enteropathy
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