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15 min,再灌注48 h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。
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.
出处
《山东大学学报(医学版)》
CAS
北大核心
2012年第4期61-65,75,共6页
Journal of Shandong University:Health Sciences
基金
山东省自然科学基金资助项目(Y2006C86)
关键词
缺血预处理
脑缺血耐受
血管内皮生长因子
脑梗死
Ischemic preconditioning
Brain ischemic tolerance
Vascular endothelial growth factor
Cerebral infarction