FEATURES OF SYSTEMIC SCLEROSIS INDUCTION IN EXPERIMENTAL CONDITIONS
Summary. The purpose: to describe the features of the pathogenesis of lesions of the respiratory portion of the lungs in the experimental induction of systemic sclerosis (SSc). Object and methods. An experimental group of animals from 25 adult Wistar rats was formed to simulate SSc; the control group consisted of 20 individuals. 0.5 ml of 5% sodium hypochlorite solution (NaClO) was injected subcutaneously three times a week for 6 weeks. Animals of both groups were euthanized 8 weeks after the start of the experiment. The study determined the level of oxyproline, catalase, TBA-active products, medium weight molecules (MWM) and diene conjugates (DC) The concentration of surfactant protein D (Elabscience SP-D ELISA-Kit), vascular adhesion molecule-1 (Elabscience VCAM-1 ELISA-Kit) and interleukin 13 (Elabscience IL-13 ELISA-Kit) was determined by enzyme-linked immunosorbent assay. To describe the morphological changes, lung tissue samples were examined by light microscopy (Leica DM750, magnification x200) by standard staining techniques (hematoxylin and eosin). Results. In the experimental group of animals, the level of catalase was lower compared to the control (9.69 ± 0.67 g / l and 11.1 ± 0.87 g / l, respectively, p <0.05). In contrast, the rate of TBA-active products was higher in the experimental group (4.3 ± 0.26 nmol / ml and 3.85 ± 0.23 nmol / ml, respectively, p <0.05) as well as the level of MWM (0.261 ± 0.027 and 0.247 ± 0.031, p <0.05) and DC (0.0139 ± 0.0032 and 0.0060 ± 0.0011, p <0.05). The concentration of oxyproline in the blood plasma of laboratory animals from the experimental group was higher compared to control animals (34.03 ± 5.01 μmol/l and 33.23 ± 2.4 μmol / l, p <0.05). Higher IL-13 (136.4 ± 56.23 and 9.43 ± 4.01, p <0.05), VCAM-1 (91.25 [IQR 85.63–143.75] and 17.35 ± 7.47, p <0.05) and SP-D (490.20) were also observed in the experimental group. [IQR 228.75–568.73] and 70.13 ± 33.21, p <0.05). Histological analysis of lung biopsies of the experimental group of animals showed violations of the morphological structure characteristic of nonspecific interstitial pneumonia. The assessment of the severity of fibrosis on the Ashcroft scale was significantly higher in the experimental group (3.7 ± 0.6) compared with controls (0.6 ± 0.1) (p <0.05). Conclusions. The described model of experimental induction of SSc allows to characterize pathogenetic mechanisms of typical morpho-functional disturbance of respiratory portion of the lungs.
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