Study of the Neurogliocyte Apoptosis in Hippocampus under Cerebral Ischemia-reperfusion in Diabetic Rats

Objective To explore the molecular mechanism of the neurogliocytes damage with cerebral ischemia-reperfusion in the diabetic rats.Methods Ninety-six adult SD rats were randomizedly allocated into four groups including sham operation group,normoglycemia operation group,diabetes operation group and PD98059 diabetes operation group(24 rats per group).Streptozocin was used to induce diabetes,and a whole cerebral ischemia model of diabetic rat was established by the bilateral vascular occlusion combined with bloodletting.H and E staining was used to observe morphological changes,and TUNEL was used to detect the apoptosis of CA2 and CA4 in the hippocampus region of diabetic cerebral ischemia injury by PD98059 and ERK1/2.Results The neuroglial apoptosis of CA2 and CA4 in the hippocampus region among the diabetes groups was significantly higher at 15 minutes after ischemia and 1h,3h,6h after reperfusion compared with the normoglycemia groups(P0.05).The neurogliocyte apoptosis expression in PD98059 groups was significantly lower than it in the diabetes groups at each time point of cerebral ischemia and reperfusion(P0.05).Conclusion Hyperglycaemia can increase the neurogliocytes damage of CA2 and CA4 in rat with cerebral ischemia-reperfusion injury.Phosphorylation of ERK1/2 which was induced by hyperglycaemia possibly led to the neurogliocyte apoptosis of CA2 and CA4 in the hippocampus.