论文部分内容阅读
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 investigate the effect of ischemic preconditioning (IP) on the expression of vascular endothelial growth factor (VEGF), matrix metalloproteinase-9 (MMP-9) and microvessel density (MVD) after focal cerebral infarction and to explore the protective mechanism of IP. Methods The focal cerebral ischemia middle cerebral artery occlusion model (MCAO) was established by thread occlusion method. MCAO 10min was used as IP and the model of permanent middle cerebral artery infarction (PMCAO) was made 48h after IP. Water volume, observe the pathological changes of brain tissue, detect the expression of VEGF and MMP-9 and the change of brain microvessel density (MVD). Results IP significantly reduced the neurological and histological damage of PMCAO rats, decreased the expression of MMP-9 and decreased the expression of brain edema, VEGF and the increase of microvessel density in PMCAO rats. Conclusions IP has obvious protective effect on the subsequent PMCAO, induces the production of cerebral ischemic tolerance (IT), and the neuroprotection of cerebral IT is closely related to the angiogenesis after cerebral infarction.