Phosphorylized ERK1/2 is upregulated in diabetic rats after global cerebral ischemia-reperfusion injury

Objective To explore the expression of extracellular signal-regulated kinase 1/2 (ERK1/2) in the hippocampus CA4 region of diabetic rats after global cerebral ischemia-reperfusion injury. Methods Diabetic rat was established by intraperitoneal injection of streptozocin (STZ) and then global cerebral ischemia model was induced by bilateral clamping of the carotid arterial plus hypotension by withdrawing blood. Apoptosis of neuron and expression of the phosphorylation of ERK1/2 (P-ERK1/2)were observed in the hippocampus CA4 region of diabetes operation groups (DCI) and normoglycemia operation groups (NCI) by TUNEL,immunohistochemistry at 15 min after ischemia and at 1 h after reperfusion. Results Compare with the NCI,neuronal apoptosis of DCI was significantly higher at each time point of cerebral ischemia and reperfusion in the hippocampus CA4 (P0.05),and the expression and activation of P-ERK1/2 was up-regulated and was significantly higher than that in NCI at 1 h after reperfusion in the hippocampus CA4 (P0.01). Conclusion Diabetes could augment the neuronal injury after cerebral ischemia-reperfusion. Hyperglycemia-exaggerated cerebral ischemic injury is related to the activation of ERK1/2.