Abstract
was resected the uterine horn which was dissected along its sagittal axis, the flap was sutured to the parietal peritoneum with the endometrial surface. Before the surgery the rats were estrogenised with folliculinum during 5 days. The statistical processing was conducted by the non-parametric methods, the software tools of Statistica 7.0 (StatSoft Inc., USA) were used. There was determined that the growth of enometrioid ectopies was slowed in the conditions of the blockade of endometrioid ectopies and the distrophic changes in transplanted tissue were enhanced. The obtained data are the evidence of the possible use of demethylating agents on the endometrial foci. There seems the system of DNA methylation could regulate not obly the proliferative processes but also the development of pathomorphogenetic changes in the endometrial ectopies, associated with the disorders of the architectonics of the cellular structures manifested as the hyperplasia of endometrium. However the mechanisms of this impact could be realized through the genes responsible for morphogenesis (PTEN, Atk, homeobox, aPKC, Wnt-system), including the genes of growth factors (platelet-derived growth factor (PDGF), fibroblast growth factor-2 (FGF-2), epidermal growth factor (EGF) etc.). To clarify the peculiarities of the impact of DNA methylation on the pathomorphogenetic processes in endometriosis the further research is necessary.
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