糖尿病大鼠脑缺血再灌注海马CA4区神经元中磷酸化ERK1/2的表达上调  

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

作　　者：马轶[1] 景丽[1] 郭凤英[1] 张建中[1] 

机构地区：[1]宁夏医科大学基础学院病理学系,银川750004

出　　处：《第三军医大学学报》2009年第23期2312-2314,共3页Journal of Third Military Medical University

基　　金：国家自然科学基金(30560044);宁夏高等学校科研基金(2005055);宁夏医科大学面上项目(2006009)~~

摘　　要：目的探讨细胞外信号调节激酶1/2(extracellular signal-regulated kinase1/2,ERK1/2)在糖尿病脑缺血再灌注大鼠海马CA4区神经元表达的意义。方法在链脲佐菌素性糖尿病大鼠脑缺血再灌注模型基础中,应用TUNEL、免疫组化方法观察糖尿病脑缺血组与正常血糖脑缺血组在全脑缺血15min、再灌注1h海马CA4区神经元凋亡和磷酸化ERK1/2(P-ERK1/2)的表达变化。结果糖尿病脑缺血组在缺血15min、再灌注1h海马CA4区神经元凋亡发生率均明显高于正常血糖脑缺血组(P<0.05);糖尿病脑缺血组各时间点磷酸化ERK1/2明显增高,于再灌注1h明显高于正常血糖组(P<0.01)。结论糖尿病加重脑缺血再灌注神经元的损伤,其机制可能与ERK1/2的激活有关。Objective To explore the expression of extracellular signal-regulated kinase 1/2 （ERKI/2） in the hippocampus CA4 region of diabetic rats after global cerebral isehemia-reperfusion injury. Methods Diabetic rat was established by intraperitoneal injection of streptozoein （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 normoglyeemia operation groups （NCI） by TUNEL, immunohistochemistry at 15 rain 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 （P 〈 0.05） , 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 （P 〈0.01 ）. Conclusion Diabetes could augment the neuronal injury after cerebral ischemia-reperfusion. Hyperglycemia-exaggerated cerebral ischemic injury is related to the activation of ERK1/2.

关 键 词：糖尿病 脑缺血再灌注损伤 细胞外信号调节激酶(ERK1/2) 海马 凋亡 

分 类 号：R322.81[医药卫生—人体解剖和组织胚胎学] R394.2[医药卫生—基础医学]