摘要
目的研究缺血预处理(IP)对局灶性脑梗死后血管内皮生长因子(VEGF)、基质金属蛋白酶-9(MMP-9)表达以及微血管密度的影响,探讨IP脑保护作用机制。方法利用线栓法建立局灶性脑缺血大脑中动脉闭塞模型(MCAO),MCAO 10min作为IP,IP后48h制作永久性大脑中动脉梗死(PMCAO)模型,进行神经功能评分、测定脑组织含水量、观察脑组织病理改变、检测VEGF及MMP-9表达和脑组织微血管密度(MVD)变化。结果 IP显著减轻PMCAO大鼠神经功能及组织学损害,降低PMCAO后MMP-9的表达,减轻脑水肿,VEGF表达及微血管密度增加。结论 IP对其后PMCAO有明显的保护作用,能诱导脑缺血耐受(IT)的产生,脑IT的神经保护作用与脑梗死后血管再生密切相关。
Objective To study the effect of ischemic preconditioning（IP） on expressions of vascular endothelial growth factor（VEGF） and matrix metalloproteinase-9（MMP-9） and the micro-vessel density（MCV） after focal cerebral infarction in rats,and to explore the mechanism of neuro-protection of IP on subsequent focal cerebral infarction.Methods Transient middle cerebral artery occlusion（MCAO） for 10 min was used as IP,and reperfusion for 48 h was carried out after IP and before permanent MCAO（PMCAO） to produce ischemic tolerance（IT）.Nerve function score,brain water content,pathological changes in cerebral tissues,expressions of VEGF and MMP-9,and MVD were detected.Results IP significantly reduced neurological and histological injuries after PMCAO.Immunohistochemical examination revealed that 24 h after PMCAO,expression of MMP-9 in the IP experimental group was lower than that in the control group and the sham operated group,while VEGF expression and MVD were higher.Brain edema was reduced in the IP experimental group.Conclusion IP can provide significant brain protection for subsequent PMCAO and induces IT in the brain.It provides dramatic protection through promoting angiogenesis.
出处
《山东大学学报（医学版）》
CAS
北大核心
2011年第3期8-12,共5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
脑缺血发作
短暂性
明胶酶B
血管内皮生长因子
血管再生
Ischemic preconditioning
Ischemic attack
transient
Gelatinase B
Vascular endothelial growth factor
Angiogenesis
