THE INFLUENCE OF MESENCHYMAL STEM CELLS ON THE DYNAMICS OF REGULATOR OF ENDOTHELIAL PROLIFERATION EXPRESSIONS IN THE BRAIN STRUCTURES OF RATS WITH EXPERIMENTAL ALZHEIMER-TYPE DEMENTIA

Abstract

Background. Despite numerous studies, the assessment of the functional state of the vascular endothelium by determining the localization of cells, producers of the endothelial proliferation factor, and measuring the intensity of its production in the brain of rats with dementia of Alzheimer type is of great relevance. Objective: to investigate the impact of mesenchymal stem cells on the functional state of the endothelium of brain vessel in rats with Alzheimer-type dementia by assessing the optical density of brain structures expressing the endothelial proliferation factor. Results. In neurons of the CA1 zone of the hippocampus in gr. SС-14 and in In SС-28, SС-28-MSC, the optical density of cytoplasm marked by endothelial proliferation factor, compared to the control, was 3.6, 1.5, and 2.0 times lower, respectively, and in cortical neurons it did not differ from the control level. After injections of mesenchymal stem cells in all studied groups, there was a decrease in the optical density of labeled factor proliferation of the endothelium of the cytoplasm of cortical neurons and more significantly - in hippocampus neurons (especially in the SС-14-MSC group). Conclusions. In rats with scopolamine-induced dementia of the Alzheimer's type, after 14 days of the "regeneration" period, compared to controls the expression level of vascular factor in hippocampal neurons was significantly lower than that in cortical neurons, which is associated with their greater degree of damage depending on the duration of scopolamine administration, Less active production and more significant reception of endothelial proliferation factor by endotheliocytes was accompanied by a decrease in the optical density of the correspondingly labeled plasma. The introduction of mesenchymal stem cells, probably due to stimulation by the growth factors in them, leads to the activation of the proliferation of the vascular endothelium and a decrease in the synthesis of the own factor of endothelial proliferation.