Vіsnik Naukovih Doslіdžen' (Jan 2018)
EXPRESSION OF S-100 PROTEIN IN CEREBRAL CORTEX IN THE MODELING OF ISCHEMIA UNDER CONDITIONS OF SENSITIZATION BY BRAIN ANTIGEN AND IMMUNE CORRECTION
Abstract
Ischemia is accompanied by diffuse damage of structural elements of brain: neurons, glia and intercellular contacts. One of the markers that demonstrate glial functional processes in nervous system is the S-100 protein. The aim of the study – to learn the changes in the S-100 protein expression in the sensorimotor cortex of rats in conditions of induction of blood supply disorders in the basal region of the left carotid artery, against the background of a previous sensitization by brain antigen and with immunofun immunomodulator. Materials and Methods. In the modeling of transient ischemia against the background of previous sensitization by brain antigen and immuno-immunofluorescence immunopharm, an experiment was conducted on 185 white, sexually mature male rats weighing 260–290 g. Histologic, immunohistochemical, morphometric and statistical methods of investigation were used. Results and Discussion. The observations showed that sensitization by brain antigen induces neurodegenerative changes in the sensorimotor cortex and a slight decrease in the expression of S100 in neuropile, which is practically recovered after 22 days. However, there is an increase in this protein in the part of the gliocytes. Discirculatory changes that occurred in groups of animals with PO s and BCAs led to a slight increase in the expression of S100 in the cerebral cortex, the level of which did not significantly differ from the control values. Despite the fact that sensitization by brain antigen leads to a decrease in the expression of S100, there is an increase in neurodegenerative and destructive changes in the cerebral cortex and potentiation of the expression of S100 with the embolism of the microvessels of the brain on its background. The enhancement of the expression of S100 can be considered as systemic, since it is observed both from the side of the lesion and from the contralateral side, albeit to a lesser extent. The use of immunoaffinity in MEA s results in a less significant increase in S-100 expression and activation of astrocytes in response to transient impaired circulation in the sensorimotor cortex. Moreover, this effect, albeit less pronounced, is also observed on the contralateral side. Given that the differences in the expression of S100 with MEA s become valid from 22 (10) days after the start of the trial, it can be assumed that this is primarily due to modulation of the immune response, including the activation of the T-regulatory cell system serving in the quality of one of the neuroprotective factors that is activated after ischemia. Conclusions. Sensitization by brain antigen induces neurodegenerative changes in the sensorimotor cortex and a slight decrease in the expression of S100 in neuropile and its growth in the part of the gliocytes. Sensitization by brain antigen leads to potentiation of the growth of S100 expression in response to transient coronary disturbance in the cerebral cortex. Immunophane significantly reduces the severity of neurodegenerative changes and reduces the growth of S100 expression caused by an ischemic attack as a violation of the circulatory system in the cerebral cortex and sensitization.
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