Apoptosis is one of the twelve subtypes of physiologically programmed cell death that controls cell population, tissue volume, and homeostasis. In the endometrium, apoptosis plays a particularly important role, since it undergoes monthly desquamation, requiring the balance between anti- and pro-apoptotic which plays a key role in cyclic endometrial remodeling. The study evaluated the expression of such apoptosis factors as caspase-8, NF-, Bcl-2 in patients with chronic endometritis (CE) (n=23), external genital endometriosis (EGE) (n=20), normal endometrium (control group) (n=7). Statistically significant differences were found for all studied markers (p0.05). Increased expression of apoptosis factors probably demonstrates a high pro-inflammatory activity of the endometrium in both CE and EGE. In the case of EGE, this effect is more pronounced at the transcriptional level based on the increased expression of NF- in both glandular and stromal cells of the endometrium. This phenomenon can be explained by the systemic impact of the chronic inflammation. For CHE, despite the antiapototic activity of Bcl2, an increase in Caspase-8 expression in the endometrium may also indicate the predominance of innate immunity activation. Thus, an imbalance of pro- and anti-apoptotic factors can simultaneously induce the cytotoxic and cytoprotective interactions in the CE and CHE pathogenesis, but requires further investigations.

The energy deficit is the result of insufficient energy intake compared to its high costs. The development of energy deficiency is often associated with the desire to lose weight, a strict diet, as well as the woman's concern about her weight along with a change in eating behavior. The result of eating disorders in combination with a decrease in body weight is anorexia nervosa, accompanied by an energy deficit. Physiological changes occurring against a background of chronic energy deficiency contribute to the inclusion of compensatory mechanisms of energy conservation to provide vital physiological functions. The most frequent metabolic changes include hypoleptinemia in the presence of a decrease in the percentage of fat tissue, a decrease in triiodothyronine, and an increase in the concentrations of ghrelin, peptide YY and neuropeptide Y. The effect of energy and metabolic changes leads to suppression of the hypothalamic-pituitary-ovarian axis, gonadotropin releasing hormone secretion, with the subsequent suppression of the release of luteinizing and follicle stimulating hormones. The suppression of the hypothalamic-pituitary-ovarian axis leads to chronic estrogen deficiency, which is accompanied by the development of functional hypothalamic amenorrhea.

Introduction. One of the most challenging problems faced in gynecology is Asherman’s syndrome (AS), characterized by the formation of intrauterine adhesions, partial or complete obliteration of the uterine cavity with scar tissue, and the loss of the functional layer of the endometrium following intrauterine interventions. Treatments for AS are not always effective. This indicates a need to search and evaluate the effectiveness of new approaches to the prevention of fibrosis and stimulation of endometrial regeneration. According to ethical principles, this is possible only when simulating AS on laboratory animals. The aim of the work is to develop an etiologically adequate model of AS in Sprague Dawley rats. Materials and methods. We simulated AS in 18 female Sprague Dawley rats that were divided into 3 groups (6 rats in each). Operations were performed in the estrus phase. We made longitudinal incision of the right uterine horns, and the endometrium was scraped out to the inner layer of the myometrium with the scalpel. Groups 1 and 2 underwent only endometrial scraping. In group 3 abdominal cavities were opened on day 7 after curettage and intrauterine adhesions were destroyed with a needle inserted into the horn. Then, the standard procedure for suturing surgical wound was performed. The animals were removed from the experiment on days 7 (group 1) and 15 (groups 2 and 3) after the surgery with an overdose of ether anesthesia. The tissue samples of the operated and non-operated uterine horns were fixed with 10% buffered formalin and embedded in paraffin; the sections were stained with hematoxylin and eosin. Results. Macroscopic examination on day 7 after the surgery showed that all females had a compaction and contraction of the operated area of the uterine horn and uterine cavity fluid. On day 15, fluid collection was more pronounced. After the destruction of the uterine adhesions in rats from group 3, there was no fluid collection or it was less voluminous than in females of other groups. Histological examination showed that on days 7 and 15 after endometrial curettage, the uterine cavity and the luminal epithelium covering it were absent due to complete replacement by connective tissue. Uterine glands were not detected or were individual. On day 7 after the destruction of the adhesions and on day 15 after endometrial scraping the subjects developed a small stenosed uterine cavity lined with luminal epithelium or a larger uterine cavity containing single or multiple adhesions covered with epithelium. The number of glands was significantly smaller than in the non-operated horn. Conclusion. To simulate Asherman’s syndrome, female Sprague Dawley rats in the estrus phase were scraped out of the endometrial layer of the right uterine horn. On days 7 and 15 after surgery, the uterine cavity and luminal epithelium were absent due to complete replacement with connective tissue, which proves the formation of intrauterine adhesions and the adequacy of the obtained model. A significant difference of the original model was the destruction of the adhesions on day 7 after endometrial damage to remove excess fluid in the uterine cavity and restore uterine patency, which led to the formation of the uterine cavity and re-epithelialization on day 15. The developed model of Asherman’s syndrome can be used to develop new approaches to the prevention of adhesive process and the restoration of endometrial structure and functionality. Keywords: Asherman’s syndrome, experimental model, rat uterus, endometrial curettage, intrauterine adhesions

Introduction. The main function of the endometrium is to create the optimal environment for embryo implantation, controlled by multicomponent signaling pathways. They are modulated by progesterone and estradiol acting through related estrogen receptors (ER) and progesterone receptors (PR). Alteration in steroid hormone, follicle-stimulating hormone (FSHR), and luteinizing hormone (LGHR) receptor expression are underlying factors in the development of various reproductive disorders. Therefore, understanding the physiological features of receptors expression and localization in tissues is extremely important for a proper comprehensive assessment of the endometrial condition. Materials and methods. The expression of ER, PR, FSHR, and LGHR in endometrial samples of healthy females from different menstrual periods, who applied for assisted reproductive technologies (ART) due to male infertility, was assessed by immunofluorescence. Results. The increase in immunoreactivity of ER, PR, FSHR, and LGHR in the glands and stroma of the endometrium is initiated during the early proliferation stage and reaches its maximum during the late proliferation stage. Subsequently, ER expression in the glands and stroma gradually decreases throughout the early and middle stages of secretion; PR immunoreactivity in the stroma and FSHR and LGHR in all endometrial components persists throughout the secretion stage. Conclusion. The correspondence between the change of the studied receptors' expression and endometrium structural features at different stages of the menstrual cycle was demonstrated. The increased expression of ER, PR, FSHR, and LGHR in the endometrium at the proliferation stage coincides with the growth period of the uterine body mucosa, and the increased immunoreactivity of PR, FSHR, and LGHR during the secretion stage is associated with its decidual transformation and seems to create conditions for successful implantation and embryo development if pregnancy occurs.

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