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山东大学学报(医学版) ›› 2012, Vol. 50 ›› Issue (4): 61-.

• 论文 • 上一篇    下一篇

缺血预处理对大鼠局灶性脑梗死后VEGF、GLUT1及BAI1表达的影响

韩巨1,陈建新1,朱梅佳1,张新娟2,焉传祝3   

  1. 1.山东大学附属千佛山医院神经内科, 济南 250014; 2.山东省医学影像研究所, 济南 250021;
    3.山东大学齐鲁医院神经内科, 济南 250012
  • 收稿日期:2011-08-10 出版日期:2012-04-10 发布日期:2012-04-10
  • 通讯作者: 焉传祝(1964- ),男,教授,博导,主要从事神经肌肉病理与脑血管疾病的研究。 E-mail: czyan@sdu.edu.cn
  • 作者简介:韩巨(1970- ),男,博士,副主任医师,主要从事脑血管病介入诊疗及脑缺血神经保护的研究。
  • 基金资助:

    山东省自然科学基金资助项目( Y2006C86)

Effects of ischemic preconditioning on expression of VEGF,GLUT1 and
BAI1 in focal cerebral infarction rats

HAN Ju1, CHEN Jian-Xin1,  ZHU Mei-Jia1, ZHANG Xin-Juan2, YAN Chuan-Zhu3   

  1. 1. Department of Neurology, QianFoShan Hospital Affiliated to Shandong University, Jinan 250014, China;
    2. Institute for Medical Imaging,Jinan  250021, China;
    3. Department of Neurology, Qi Lu Hospital of Shandong University, Jinan  250012, China
  • Received:2011-08-10 Online:2012-04-10 Published:2012-04-10

摘要:

目的   研究缺血预处理(IP)对局灶性脑梗死后VEGF、GLUT1和BAI1表达的影响,探讨IP的脑保护作用机制。方法   采用大鼠局灶性大脑中动脉线栓法进行缺血预处理15min,再灌注48h后制作永久性大脑中动脉梗塞(PMCAO)模型。观察脑缺血后神经功能评分、脑组织含水量、组织病理学改变,酶标记免疫吸附测定VEGF、GLUT1及BAI1表达的变化。结果   IP显著减轻 PMCAO后大鼠神经功能损害和组织学损害,明显降低BAI1的表达,增加VEGF及GLUT1的表达,且BAI1与VEGF的表达水平呈负相关。结论   缺血预处理能诱导脑缺血耐受的产生,可能是通过改善微循环,提供必需的能量,从而对其后 PMCAO有明显的脑保护作用。

关键词: 缺血预处理; 脑缺血耐受; 血管内皮生长因子; 脑梗死

Abstract:

 Objective   To study the effects of ischemic preconditioning (IP) on expression of VEGF,GLUT1 and BAI1, and to explore the neuroprotective mechanism of ischemic preconditioning in focal cerebral infarction rats. Methods   Transient middle cerebral artery occlusion (MCAO) was done for 15 min to induce IP, and a permanent MCAO model was established at 48 h after ischemic reperfusion. Nerve function score, brain water content, pathological changes in cerebral tissue, and expressions of VEGF, GLUT1 and BAI1 were studied. Results   IP significantly alleviated neurological and histological injury after PMCAO. Immunohistochemical examination and ELISA revealed higher expression of VEGF and GLUT1 and lower expression of BAI1 in the experimental group than in the control group, with BAI1 negatively correlated with VEGF. Conclusion   IP induced brain ischemic tolerance and provided significant protection to the brain following PMCAO. This protection is probably achieved through IP-triguedmicrocirculation enhancement and energy supply.

Key words: Ischemic preconditioning; Brain ischemic tolerance; Vascular endothelial growth factor; Cerebral infarction

中图分类号: 

  • R743.31
[1] 韩巨1,孙燕1,张涛1,张新娟2,孙晋浩3. 缺血耐受大鼠局灶性脑梗死后血管再生的实验研究[J]. 山东大学学报(医学版), 2011, 49(3): 8-12.
[2] 韩巨1,孙燕1,张涛1,张新娟2,孙晋浩3. 缺血耐受大鼠局灶性脑梗死后血管再生的实验研究[J]. 山东大学学报(医学版), 2011, 49(3): 8-12.
[3] . ABCD2评分法预测短暂性脑缺血发作患者脑梗死的风险[J]. 山东大学学报(医学版), 2009, 47(9): 89-92.
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