PECULIARITIES OF THE DEVELOPMENT OF ADAPTIVE AND COMPENSATORY PROCESSES IN RATS THYROID GLAND IN EXPERIMENTAL HEPATOFIBROSIS

The aim: to evaluate the morphological substrate of adaptive and compensatory processes in the thyroid gland in experimental hepatofibrosis.

Material and methods. The work was performed on 120 white male rats weighing 180–200 g, which were co-administered with bacterial lipopolysaccharide (LPS) in a dose of 0.2 mcg/kg body weight and hepatotoxic venom – carbon tetrachloride (CTC) at a rate of 0.5 ml of a 30% CTC oil solution for 30, 60 and 90 days. Thereafter, the introduction of CTC and LPS stopped with an assessment of the morphological changes in the thyroid tissue at 7, 30 and 60 days. A histological examination resulted in an analysis of the volume fraction of extrafollicular and intrafollicular epithelium in verified hepatophybrosis and the presence of endogenous intoxication.

Results. It was found that the duration of the toxic effect affected the ability of the thyrocytes to recover and, as the periods of intoxication increased, a gradual increase in the volume fraction of the follicular and extrafollicular epithelium was observed, while after the cessation of the injection of CTC and LPS the volume fraction of thyrocytes, due to extrafollicular epithelium, which was accompanied by a microfollicular transformation of the thyroid tissue to 90 days.

Conclusion. It was established, that in modeling experimental hepatofibrosis the initial adaptation of thyrocytes consisted in changing the cell shape to cubic/prismatic, which was accompanied by resorption of the colloid on the 30th day of CTC and LPS combined administration and subsequent compensation in formation of new daughter follicles. After the termination of the toxic effect, hyperplasia of the thyrocytes was observed in the form of Sanderson’s pads, an increase in the volume fraction of the extrafollicular epithelium, which indicates the restoration of the thyroid parenchyma with the formation of proliferation centers, which can be the source of the formation of uncontrolled foci of hormonopoiesis.

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