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 areal density 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 glial cells - at the expense of increased amount of Bcl-2+-cells. On the 12lh day of the post-ischemic period the activity of antiapoptotic processes in the nerve cells increased. Streptosotocin induced diabetes during three months does not affect the areal density of Bcl-2+-nerve cells, although it increases the areal density of Bcl-2+-glial cells. 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.
