Abstract

Introduction. The high incidence of endometrial hyperplasia and the convenience of its model-ing and morphological diagnosis pose an important task for experimental medicine to develop methods or its pathogenetic correction. The paper aimed to conduct a comprehensive immunomorphological study for endometrial hyperplasia against the background of excessive estrogens, select pathogenetic therapy, and evaluate its effectiveness. Materials and methods. We used laboratory Wistar rats (n=45), which were divided into the control (n=5) and experimental (n=40) groups. We created and verified a model of endometrial hyperplasia during ovariectomy and transdermal administration of estrogens. In the experimental group, the correction with indole, meloxicam, and polyoxidonium was performed. Immunohistochemical study of the expression of proliferation markers, apoptosis, various pools of immune cells, and vascular growth factor provided data on hyperplasia development mechanisms. Results. In this model, immunophenotypic changes differ in the parts responsible for gestation (the uterine horn) and expulsion of the fetus (analogous to the human cervix). Divergent disruptions of the cell cycle of epithelial cells and the topography of immunocompetent cells were revealed. Meloxicam normalizes most of these indicators (the number of immunocompetent cells and the kinetics of cell populations); indole has an antiestrogenic effect and increases the expression of progesterone receptors; and polyoxidonium is less effective in the correction of endometrial hyperplasia. Conclusion. The dynamics of the expression of the studied markers can be recommended for diagnosis, whereas the identified effects of drugs can be used for complex pathogenetic therapy.

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