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

马轶; 景丽; 郭凤英; 张建中

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

更新时间：2026-01-09

- Phosphorylized ERK1/2 is upregulated in diabetic rats after global cerebral-ischemia reperfusion injury
- Journal of Army Medical University Vol. 31, Issue 23, Pages: 2312-2314(2009)
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  CLC： R322.81;R394.2;R587.102
- Published：2009
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马轶,景丽,郭凤英,张建中.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[J].陆军军医大学学报(原第三军医大学学报),2009,31(23):2312-2314.

　MA Yi,JING Li,GUO Feng-ying,ZHANG Jian-zhong.Phosphorylized ERK1/2 is upregulated in diabetic rats after global cerebral-ischemia reperfusion injury[J].J Amry Med Univ (J Third Mil Med Univ),2009,31(23):2312-2314.
马轶,景丽,郭凤英,张建中.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[J].陆军军医大学学报(原第三军医大学学报),2009,31(23):2312-2314. DOI：

　MA Yi,JING Li,GUO Feng-ying,ZHANG Jian-zhong.Phosphorylized ERK1/2 is upregulated in diabetic rats after global cerebral-ischemia reperfusion injury[J].J Amry Med Univ (J Third Mil Med Univ),2009,31(23):2312-2314. DOI：

摘要

目的探讨细胞外信号调节激酶1/2（extracellular signal-regulated kinase 1/2

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15 min、再灌注1 h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 h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（P0.05）；糖尿病脑缺血组各时间点磷酸化ERK1/2明显增高，于再灌注1 h明显高于正常血糖组（P0.01）。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。

Abstract

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.

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