THE RATIO OF P53-PROAPOPTOTIC AND BCL-2 ANTIAPOPTOTIC ACTIVITY IN THE HIPPOCAMPUS OF RATS WITH BRAIN ISCHEMIA-REPERFUSION AND EXPERIMENTAL DIABETES.

Abstract

The dynamics of the balance of indices of pro- and p53- Bcl-2 anti-apoptotic processes in the hippocampus of rats with experimental diabetes mellitus (DM) complicated by incomplete global cerebral ischemia-reperfusion was investigated. It is shown that p53 proapoptotic processes in animals without diabetes after 20 minutes of ischemia/l hour reperfusion in all fields of the hippocampus are activated in the background of increasing Bcl-2 antiapoptotic processes in the fields CAl, CA2, CA4 and depression of it - in the CA3 field. In the early postischemic period in rats with DM activity of the p53-proapoptotic processes in fields CAl, CA3, CA4 significantly exceeds that in non-diabetic rats (area of p53- IRM increases on 110, 60 and 27 %), and was significantly lower than that detected in CA2 field. On the 12th day of post-ischemic period, activation of apoptosis in field CAl occurs in the background of inert antiapoptotic processes, in animals without diabetes, as well as in diabetic rats, but the indicators characterizing of apoptotic activity in rats with diabetes were higher (specific contents of p53 protein and area ofp53 -IRM increases on 38 and 43 %). During this period, in the CA2 region of the non-diabetic animals, some depression of the antiapoptotic processes with a slight predominance of proapoptotic processes was detected. In the field of CA3 region of rats without diabetes, the retention of activity of proapoptotic processes and the deepening in the dynamics of depression of antiapoptotic processes were showed. In rats with DM, the oppression of both mechanisms with a significant depression of antiapoptotic processes was observed. On the 12th day of experiment in the field CA4, the most balanced relationship were detected between the studied of the processes due to their parallel and unidirectional changes both in the rats without diabetes as well as with DM. The results point on the modifying effect ofDM on susceptibility ofhippocampal fields to ischemic-reperfusion injury.