STRUCTURAL CHARACTERISTICS OF THE RAT DUODENAL MUCOSA DURING BURN INJURY TO THE SKIN UNDER THE CONDITIONS OF EXPERIMENTAL STREPTOZOTOCININ-INDUCED DIABETES MELLITUS
Abstract
The work is devoted to the study of structural features of the mucous membrane of the duodenum in case of burn injury to the skin under experimental streptozotocin-induced diabetes mellitus. The study was carried out on laboratory adult white and male rats weighing 180-210 g. The control group consisted of 21 intact animals, and the I experimental group consisted of 21 rats with experimental skin burn injury, experimental II the group consisted of 21 rats without skin burns with experimental streptozotocin-induced diabetes, the III experimental group consisted of 21 rats with skin burn and experimental streptozotocin induced diabetes. The experimental diabetes mellitus model was reproduced by administering rats streptozotocin intradermally once in a dose of 50 mg / kg. Thermal burn skin damage in rats corresponded to II - AB degree - dermal superficial 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. For morphological studies, a section of the duodenum was taken, fragments of which were processed by conventional methods of light and electron microscopy. The main criteria for assessing damage of the duodenal mucosa were the results of a study comparing histological and ultrastructural data in dynamics after 7, 14 and 21 days after a skin burn. The results of the studies showed a decrease in the number of tight contacts in the intestinal epithelial barrier of the mucous membrane of the duodenum of rats of the first and third experimental groups and the loss of order (the acquisition of a certain randomness) of their localization with increasing time after a burn injury. Defects appear in the intestinal epithelial barrier, which are potential pathways of paracelular translocation of the pathogenic contents of the duodenum. It is possible that part of this intestinal pathogenic content can be translocated and through partially damaged cells. Evidence of the latter is the presence of microbial bodies in the cytoplasm of cells with partially destroyed plasmolemma (but preserved organelles and nucleus). The adaptive mechanism for ensuring the repair of damaged enterocytes is selective autophagy, which acts as a factor in the recycling of the destroyed organelles and cytoplasmic matrix material, primarily aimed at maintaining cell viability. The initiation of autophagy associated with the development of enterocytes stress endoplasmic reticulum (ER-stress). In the enterocytes of the duodenum of rats of the third experimental group, ER-stress occurs so quickly and is accompanied by a steady spread of destruction processes in the cell, autophagy mechanisms do not have time to work, and most cells die. Thus, the absence of an autophagous reaction is a marker of the unfavorable direction of the course of post-burn structural changes in enterocytes.
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