Diabetes cerebral ischemia reperfusion rat glial cell apoptosis.docVIP

 PAGE \* MERGEFORMAT 12 Diabetes cerebral ischemia reperfusion rat glial cell apoptosis Of: Zhang Jianzhong Li Junjun Luotao Jing Li Ma Yi Guo Fengying [Abstract] Objective To investigate diabetic ischemia reperfusion injury of glial cells increased the molecular mechanism. Methods 96 adult SD rats were randomly divided into 4 groups: sham operation control group, normal blood glucose cerebral ischemia group, diabetes, lack of brain blood group, PD98059 prevent diabetes cerebral ischemia group, n = 24. with streptozotocin induced diabetes, two-vessel occlusion in diabetic rats was established by the United bloodletting global cerebral ischemia model, using the HE staining, TUNEL method to study high glucose on cerebral ischemia and reperfusion and the use of P-ERK1 / 2 inhibitor PD98059 hippocampus CA4, CA2 expression of glial cell apoptosis status. Results In diabetic rats with cerebral ischemia, the hippocampus CA4, CA2 area of #8203;#8203;glial cells in ischemic 15min, 1,3 h reperfusion increased number of apoptotic cells was higher than normal blood glucose cerebral ischemia group (P lt;0.05), using the P-ERK1 / 2 inhibitor PD98059, the In the ischemia-reperfusion glial cells at different time points the expression of apoptotic cells decreased compared with diabetic cerebral ischemia group (P lt;0.05). Conclusion hyperglycemia in Cerebral Ischemia and reperfusion injury of glial cells, high glucose-induced ERK1 / 2 phosphorylation may mediate the apoptosis of glial cells. [Keywords:] Cerebral ischemia; reperfusion; diabetes; high blood sugar; glial cells; extracellular signal-regulated kinase 1 / 2; rat Experimental studies have shown that high blood sugar can aggravate cerebral ischemia reperfusion injury [1]. Ischemic brain damage mainly in two forms, namely, necrosis and apoptosis, but apoptosis is delayed ischemic brain areas onset of the main forms of neural cell death [2]. The exact mechanism of neuronal apoptosis is not clear, in recent y