Reaction of Bcl-2+ cells of the parietal lobe cortex of rats with experimental diabetes mellitus to ischemia-reperfusion

Abstract

The peculiarities of anti-apoptotic mechanisms in the nerve and glial cells of the parietal lobe cortex are studied by the density changes of Bcl-2+-cells location and concentration of Bcl-2 protein in them in rats with diabetes mellitus in the dynamics of ischemic-reperfusion cerebral injury. Bilateral carotid ischemia-reperfusion is found to inhibit anti-apoptotic reaction of nerve cells of the parietal lobe cortex in the early and late post-ischemic periods at the expense of decreased number of Bcl-2+-cells and concentration of Bcl-2 protein in them. In glial cells during the early period of ischemic-reperfusion injury the activity of anti-apoptotic processes intensifies to some extent by means of increased concentration of Bcl-2 protein in them, and on the 12th day the activity of anti-apoptotic processes decrease at the expense of reduced amount of Bcl-2+-cells and the content of Bcl-2 protein in them. Three-month streptozotocin-induced diabetes increases the location density of positive by protein Bcl-2 nerve cells in the parietal lobe cortex without influencing on the location density of Bcl-2+-glial cells and concentration of Bcl-2 protein in them. 20-minute ischemia with one-hour reperfusion in animals with diabetes mellitus considerably enhances anti-apoptotic potential of glial cells in the parietal lobe cerebral cortex at the expense of increased amount of Bcl-2+-cells and the concentration of Bcl-2 protein in them without reliable effect on these indices in nerve cells. On the 12th day of ischemic-reperfusion period in rats with diabetes mellitus, the intensity of anti-apoptotic processes in general decreases both in nerve and glial cells of the parietal lobe cortex.