Abstract
The aim of the present work was to identify the role of cycloferon in the apoptosis of cells in the neurosecretory centers of the hypothalamus in young and old mice in conditions of immobilization stress. Apoptotic cells were identified by staining with ethidium bromide. The optical density of the detection product of the antiapoptotic protein Bcl-2 was also studied in cells of the supraoptic and paraventricular (PVN) nuclei. Cycloferon was found to decrease the level of apoptosis in the neurosecretory centers of the hypothalamus via a Bcl-2-independent pathway. Administration of cycloferon before stress had no effect on the number of apoptotic cells, except in the PVN of old mice, where apoptosis was inhibited.
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