Effect of Gonadotropin-Releasing Hormone Antagonist on the Expression Patterns of Insulin-Like Growth Factor 1, Androgen Receptor, and Luteinizing Hormone Receptor in an Experimental Rat Model of Functional Ovarian Cysts.

We studied the expression of insulin-like growth factor 1 (IGF-1), androgen receptor (AR) and luteinizing hormone receptor (LHR) in the ovaries under the conditions of the modeling and subsequent treatment of functional ovarian cysts with gonadotropin-releasing hormone antagonist (ant-GnRH). The intensity of IGF-1, LHR, and AR expression in the generative elements of rat ovaries changed under conditions of functional ovarian cysts simulation, as well as during treatment with ant-GnRH. In both experimental groups, the expression levels of the studied markers in preantral follicles and epithelial lining of cysts were found to be related to the number of growing follicles and cysts. A divergence of LHR and AR expression indices and a more pronounced decrease in the number of cystic cavities were observed in the group receiving ant-GnRH. These changes demonstrate a positive effect of ant-GnRH on intra-ovarian regulatory factors and a therapeutic effect in functional ovarian cysts.

Morphofunctional State of the Ovaries in Rats with Experimental Model of Functional Cysts and Their Treatment with Gonadotropin-Releasing Hormone Antagonist.

The morphofunctional features of the ovaries were evaluated in rats with functional ovarian cysts model treated with gonadotropin-releasing hormone antagonist. Administration of the antagonist significantly (p=0.009) reduced the number of cysts and the growth of follicles in the ovaries. The obtained results attest to a possibility of successful treatment of functional ovarian cysts with gonadotropin-releasing hormone antagonist.

Changes in the synaptoarchitectonics of the retina after light-induced damage and their correction with antioxidants of plant origin.

Changes in contacts between neurons in the internal reticular layer of the retina were studied in white rats 7 and 30 days after exposure to high-intensity light. Osmium preparations on day 7 demonstrated synapse destruction, predominantly of the "light" type of. Contrasting with phosphotungstic acid was used to study juxtamembrane formations of the system of subsynaptic units, i.e., dense projections and postsynaptic thickenings of synapses. The action of light was found to induce destructive changes in synapses, with decreases in the number density of synapses due to functionally active asymmetric contacts. On day 30 after light-induced damage, there was a significant increase in the number density of symmetrical contacts and a decrease in the content of asymmetric mature synapses. Courses of ascovertin and carovertin before and after exposure to light produced different degrees of restriction of synapse destruction and activated repair mechanisms mediated by hypertrophy and neosynaptogenesis. Carovertene had the greater effect.

[Changes of synaptoarchitecture of the retina after the light-induced damage and their correction by plant antioxidants].

The changes of interneuronal contacts in the internal reticular layer of albino rat retina were studied 7 and 30 days after the exposure to high intensity light (6000 Lux for 6 h). In osmicated preparations, the "light" type of synapse destruction was predominant 7 days after the light-induced damage. Using the contrasting by phosphotungstic acid, paramembrane structures of the system of subsynaptic units--dense projections and postsynaptic condensations of synapses--were studied. It was found that the exposure to high intensity light resulted in the destructive changes of synapses and the decrease of their numeral density at the expense of the actively functioning symmetric contacts. 30 days after the light-induced damage, the numeral density of symmetric contacts was significantly increased, while the content of symmetric mature synapses was decreased. Course administration of ascovertine and carovertine before and after the exposure to light was found to have a differential effect on limiting the destruction of the synapses and on the activation of the repair mechanisms which are realized due to the hypertrophy and neosynaptogenesis. The highest effect was found after carovertine administration.