磷酸化ERK1/2在糖尿病大鼠脑缺血再灌注损伤中的表达意义
Expression of the phosphorylation of ERK1/2 in diabetic rats with global cerebral ischemia-reperfusion injury
马轶 1景丽 1郭凤英 1张建中1
作者信息
- 1. 宁夏医科大学基础学院病理学教研室,宁夏,银川,750004
- 折叠
摘要
目的:探讨细胞外信号调节激酶1/2(ERK1/2)在糖尿病脑缺血再灌注大鼠神经元中表达的作用.方法:采用链脲佐菌素(STZ)诱导和双血管阻塞联合放血法建立糖尿病大鼠全脑缺血模型,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15 min、再灌注1,3h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15 min、再灌注1,3 h各时间点海马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);糖尿病脑缺血组在各时间点磷酸化ERK1/2均有较高表达,于再灌注1,3 h明显高于正常血糖组(P<0.01).结论:ERK1/2可能参与并介导了糖尿病加重的脑缺血再灌注神经元的损伤.
Abstract
AIM: To explore the expression of extracellular signal-regulated kinase 1/2 (ERK1/2) at neuron of diabetic rats with global cerebral ischemia-reperfusion injury. METHODS: Establish diabetic rat of global cerebral ischemia model by induction with streptozocin(STZ) and 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 hippocampus CA4 region of diabetes operation groups (DCI) and normoglycemia operation groups (NCI) by TUNEL, immunohistochemistry at 15 min after ischemia and at 1,3 h after reperfusion. RESULTS: Compared with the NCI, neuronal apoptosia of DCI was significantly higher at each time point of cerebral ischemia and reperfusion in hippocampus CA4 ( P ＜ 0.05); the expression and activation of P-ERK1/2 was up-regulated and was significantly higher than NCI at 1, 3 h after reperfusion in hippocampus CA4(P ＜ 0.01). CONCLUSION: ERK1/2. could participate and mediate the aggravated neuronal injury of diabetes after Cerebral Ischemia-Reperfusion.
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Key words
diabetes/cerebral ischemia-reperfusion injury/extracellular signal-regularted kinase1/2/hippocampus/apoptosis引用本文复制引用
基金项目
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)
出版年
2009
NETL
NSTL
维普
万方数据