Patologìâ (Dec 2016)
The modifying effect of diabetes mellitus on the reaction of р53-dependent proapoptotic mechanisms of hippocampus of rats in dynamic of ischemic-reperfusion damage of brain
Abstract
A few studies are devoted to mechanisms of death of hippocampal cells under conditions of complications of diabetes mellitus (DM) with acute disorders of cerebral circulation, although the frequency of ischemic-reperfusion brain damage on a background of diabetes is much higher than that in the general population. The objective of research is to study the state of p53-dependent proapoptotic mechanisms in the hippocampal fields in the dynamic of ischemic-reperfusion brain damage in rats with experimental diabetes mellitus. Materials and methods. In neurons of hippocampal fields of rats with experimental DM content of p53 protein was studied by immunofluorescence using monoclonal antibodies in dynamic of incomplete global brain ischemia-reperfusion. The diabetes mellitus was modeled by single intraperitoneal injection of streptozotocin (Sigma, USA, 60 mg / kg). The results were estimated after a 20-minute carotic ischemia combined with one-hour reperfusion and on the 12th day of postischemic period. Results. After 20 minutes of ischemia / one hour reperfusion, in rats without DM and with DM, the activity of p53 proapoptotic processes increased in all the fields of hippocampus, only in the last group of rats its indices significantly exceed these are in hippocampal fields CA1, CA3, CA4 of rats without diabetes. On the 12th day of postischemic period in hippocampal fields CA1-CA3 of rats without diabetes the proapoptotic activity remains high, and in the field CA4 returns to normal level. In this period, in rats with diabetes activity of p53 proapoptotic processes remains increased in the field of CA1, returns to the level in rats with diabetes in the field of CA2, and decreases – in the fields CA3 and СA4. Conclusions. Diabetes mellitus quantitatively modifies the reaction of product of proapoptotic gene of p53 protein to the ischemic-reperfusion injury of the brain in the early postischemic period in the hippocampal fields CA1-CA3 and qualitatively – on the 12th day of postischemic period in hippocampal fields CA2-CA4.
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