EARLY AND DELAYED REACTION OF BCL-2+ PROTEIN IN THE NERVE AND GLIAL CELLS OF THE FRONTAL LOBE CEREBRAL CORTEX IN RATS WITH EXPERIMENTAL DIABETES MELLITUS ON ACUTE CIRCULATORY

Abstract

The activity of antiapoptotic processes in neurons and glial cell sof the frontal lobe cerebral cortex has been studied according to the change sof Bcl-2+ protein content in rats with streptosotocin induced diabetes mellitus in the dynamics of ischemic-reperfusion cerebral injury. 20 minute ischemia with one hour reperfusion in animals without diabetes mellitus concerning the control has been found to intensify antiapoptotic potential of the nerve cells of the frontal lobe cortex at the expense of increased general content of Bcl-2+ protein, and glial cells — at the expense of increased amount of Bcl-2+-cells. On the 12th day of the post-ischemic period the activity of antiapoptotic processes in the nerve cells remains increased, and in glial cells it decreases by means of reducing concentration of Bcl-2+ protein. Streptosotocin induced diabetes during three months does not affect the areal density of Bcl-2+-nerve cells and the content of Bcl-2+ protein in them, although it increases the areal density of Bcl-2+-glial cells considerably with less substantial decrease of Bcl-2+ protein content in them as compared to the appropriate indices in rats without this pathology. The nerve cells of the frontal lobe cerebral cortex of rats with diabetes mellitus in early and delayed ischemic-reperfusion periods present the activation of antiapoptotic mechanisms at the expense of increase of both the number of Bcl-2+-cells and the content of Bcl-2+ protein in them; in Bcl-2+-glial cells on the 12th day of the experiment the content of Bcl-2+ protein decreases inconsiderably against their unchanged amount.