The features of proliferative processes in the thyroid gland of the Wistar rat’s young offspring after intrauterine action of dexamethasone

Abstract

The urgency of the problem of thyroid disease in children and adolescents in Ukraine has existed for a long time. In clinical practice, synthetic glucocorticoids such as dexamethasone are used to accelerate fetal maturation in pregnant women at risk of preterm birth. In humans and other mammals, a surge of cortisol in the body causes structural and functional changes in the tissues of the fetus, preparing it for childbirth and extrauterine life, but they can have longterm consequences in the structural organization of organs remotely postnatally. Unfortunately, despite the large number of studies on the effects of glucocorticoids on the fetus, there is almost no data on the prenatal effect of dexamethasone on the processes of proliferation in the thyroid gland. In the experiment animals were divided into 3 groups(108 Wistar rats): I - intact rats; II - control - animals which, on the 18th day of the dated pregnancy transuterine, transdermal, subcutaneously in the interscapular area was injected with 0.9% saline in the amount of 0.05 ml; III - experimental group - animals, which injected the same type as a control with a solution of dexamethasone at a dose of 0.05 ml at a dilution of 1:40 intrauterinely on the 18th day of pregnancy (Ukrainian patent №112288) . The thyroid gland with the tracheal area was removed on the 1-21 days of life. Immunohistochemical study was performed according to the protocol recommended for a particular antibody manufacturer. Used monoclonal antibodies ki-67 (Ki-67), Fox-1 Antibody (A-12) - to assess proliferative activity, the company Santa Cruz Biotechnology, Inc. (USA). The thyroid infant rats, which prenatally exposed to dexamethasone, is structurally represented by chaotically located follicles of different diameters with a predominance of large with desquamated cells in the lumen, and proliferative changes aimed at forming extrafollicular which is confirmed immunohistochemically by the presence of Ki-67 positive cells. Intracellularly, proteinsynthesizing organelles of thyrocytes also proliferate, to which there is a clear cytoplasmic and nuclear reaction with Fox-1 antibodies. Proliferative processes in the thyroid of the experimental group are stabilized while maintaining the morphological structure of the hypofunctional type, and remain lower compared to the control and intact groups. Morphological signs of functional tension of the thyroid gland animals exposed prenatally to dexamethasone, which correlate with a decrease in proliferative activity, indicate a functional compensatory response of synthetic and hormone-producing function, but suppression of proliferative processes, despite the slight manifestations. The thyroid gland of morphological hypofunctional type after prenatal action of dexamethasone in young rats, indicates an adaptogenic compensatory response and morpho-functional immaturity of the organ during this period, which may be the basis for provoking the preservation of such morphogenetic factors under the influence of stressors.