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首页|期刊导航|神经损伤与功能重建|缺血后处理对脑缺血再灌注损伤后ERK1/2和Akt磷酸化及神经细胞凋亡的影响

缺血后处理对脑缺血再灌注损伤后ERK1/2和Akt磷酸化及神经细胞凋亡的影响

邢变枝 陈晖 张苏明

神经损伤与功能重建2012,Vol.7Issue(3):175-179,5.
神经损伤与功能重建2012,Vol.7Issue(3):175-179,5.DOI:10.3870/sjsscj.2012.03.006

缺血后处理对脑缺血再灌注损伤后ERK1/2和Akt磷酸化及神经细胞凋亡的影响

Effects of Ischemic Post-condtioning on Activation of ERK1/2 and Akt and Neuronal Apoptosis in Rats with Cerebral Ischemia Reperfusion Injury

邢变枝 1陈晖 2张苏明3

作者信息

  • 1. 武汉大学人民医院放射科,武汉,430060
  • 2. 武汉大学人民医院泌尿外科,武汉,430060
  • 3. 华中科技大学同济医学院附属同济医院神经内科,武汉,430030
  • 折叠

摘要

Abstract

Objective: To investigate the effects of ischemic post-condtioning on ERK1/2 and Akt activation and neuronal apoptosis in rats with cerebral ischemia reperfusion injury. Methods: SD rat with focal ischemic reperfusion was induced by intraluminal middle cerebral artery occlusion (MCAO) with a nylon monofilament suture. Ischemic animals were randomly assigned to 3 groups(w = 24) , the sham group, I/R group and Postcond group. In Postcond group, the animals with MCAO were further subject to postconditioning (6 cycles of 30s ischemia and 30s reperfusion) after MCAO. The phosphorylation of Akt and ERK1/2 in the cortex was measured by Western Blot. The neuronal apoptosis was detected by TUNEL staining. Results: Postcond treatment significantly increased phosphorylation of Akt and ERK1/2 at 10 min, 30 min, and 6 h after reperfusion. At 24 h after reperfusion, the rats in the Postcond group showed much less TUNEL positive cells in the cortex than those in the I/R group. Conclusion: Ischemic post-conditioning decreases apoptosis and improves neurological functions, perhaps which by increasing levels of Akt and ERK1/2 activation in cerebral I/R injury.

关键词

缺血后处理/ERK1/2/Akt/脑缺血再灌注损伤

Key words

ischemic post-condtioning/ ERK1/2/ Akt/ cerebral ischemia reperfusion injury

分类

医药卫生

引用本文复制引用

邢变枝,陈晖,张苏明..缺血后处理对脑缺血再灌注损伤后ERK1/2和Akt磷酸化及神经细胞凋亡的影响[J].神经损伤与功能重建,2012,7(3):175-179,5.

基金项目

国家自然科学基金(No.30901552,30901494) (No.30901552,30901494)

神经损伤与功能重建

OACSTPCD

1001-117X

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