Abstract

Background. In recent years, the prevalence of thyroid pathologies of various origins among children in the world has reached a significantly high level. The use of glucocorticoids during pregnancy remains a debatable issue in obstetrics today, as they can both positively and negatively affect the processes of organ morphogenesis and be the cause of pathological conditions in the postnatal period. Objective: to establish the features of morphofunctional transformations during the morphogenesis of the thyroid gland of the offspring of rats at an early age in normal and after intrauterine action of dexamethasone. Methods. 108 thyroid glands of rats of 3 experimental groups were microscopically examined using histological and immunohistochemical methods, followed by statistical processing of the obtained results. Results. Against the background of high levels of total follicular thyrocytes per 1 day of life in animals that received prenatal dexamethasone, cytoplasmic expression of TgAb was expressed, which correlated with the indicators of nuclear and cytoplasmic Fox-1 expression. From the 7th to the 11th day, a decrease in the total number of thyrocytes per unit area was observed due to the accumulation of colloid in the follicles, an increase in Fox-1 cytoplasmic expression and a decrease in nuclear expression, against the background of increased proliferative activity. By day 21, Fox-1 cytoplasmic and nuclear expression were almost identical. There was a decrease in the intensity of TgAb expression in the cytoplasm of thyrocytes and its expression in the colloid, a decrease in the number of Ki-67 positive thyrocytes per conditional unit area compared with the previous observation period. Conclusion. It was found that prenatal exposure of dexamethasone causes the offspring accelerate the development of morphological structures of the thyroid gland, but functionally they are in a state of stress of both the synthesizing apparatus and the process of hormone excretion, which is expressed in the imbalance of immunohistochemical expression of Fox-1 and TgAb. Such thyrocytes with signs of disturbances in synthetic activity desquamate into the lumen of the follicles, while on the 11th day we compensatory increase in the proliferative activity of the thyroid epithelium.

Highlights

  • The thyroid gland is important for the normal functioning of the body, and is the largest endocrine organ, which among the endocrine glands developed as the first in the process of embryogenesis

  • It was found that prenatal exposure of dexamethasone causes the offspring accelerate the development of morphological structures of the thyroid gland, but functionally they are in a state of stress of both the synthesizing apparatus and the process of hormone excretion, which is expressed in the imbalance of immunohistochemical expression of Fox-1 and TgAb

  • Pathology of the thyroid gland over the past 20 years has been ranked first positions among endocrine diseases of children in Ukraine and all over the world, and it forms the picture of the prevalence of all endocrine diseases, as it occupies a total of 58.0% of their structure, mainly due to disorders of organ morphogenesis and immune neuro-endocrine imbalance [1

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Summary

Introduction

The thyroid gland is important for the normal functioning of the body, and is the largest endocrine organ, which among the endocrine glands developed as the first in the process of embryogenesis. The action of thyroid hormones is variously directed at all metabolic processes, functions of many organs and tissues, including fetal development, growth processes and tissue differentiation [3, 4, 5]. The thyroid gland has a high sensitivity to exogenous and endogenous influences and the ability to morphologically rearrange tissue [6, 7]. Synthetic glucocorticoids such as dexamethasone are used to accelerate fetal maturation in pregnant women at risk of preterm birth [8, 9, 10]. Glucocorticoids mimic the effects of endogenous elevation of plasma cortisol, which is usually observed in the fetus, close to the date of birth [11]. 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 [12, 13, 14]

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