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目的探讨脑缺血区血管新生和神经功能缺失修复的关系以及选择较理想的外源性干预途径增加脑缺血区血管新生。方法选择240只SD大鼠分为假手术组、缺血对照组、缺血加VEGF腹腔注射组、缺血加血管内皮祖细胞移植组和缺血加血管内皮因子单克隆抗体组,在1、3、7、14、30、60 d观察各组脑缺血及周边区的血管密度和大鼠的电生理指标(体感诱发电位和运动诱发电位)及行为学(感觉损伤移交实验、轮转跑步机运动功能测定和mNSS改良神经功能评分)。结果缺血加VEGF腹腔注射组、缺血加血管内皮祖细胞移植组的新生血管密度除1 d外其他各时间点均高于缺血对照组(P<0.05),缺血加血管内皮因子单克隆抗体组在后5个时间点新生血管密度小于缺血对照组(P<0.05)。缺血加VEGF腹腔注射组、缺血加血管内皮祖细胞移植组和缺血加血管内皮因子单克隆抗体组在7 d后体感诱发电位和运动诱发电位与缺血对照组有统计学差异(P<0.05)。与缺血对照组相比,缺血加VEGF腹腔注射组、缺血加血管内皮祖细胞移植组和缺血加血管内皮因子单克隆抗体组在3 d后行为学评分有统计学差异(P<0.05)。结论通过外源性干预脑缺血模型大鼠缺血区血管新生,可以影响神经功能缺失的修复;且单次移植血管内皮祖细胞与VEGF多次注射用药可以达到相同的效果。
Objective To explore the relationship between angiogenesis and neurological deficit repair in cerebral ischemic area and to select the more ideal exogenous intervention pathway to increase angiogenesis in ischemic area. Methods 240 Sprague-Dawley rats were randomly divided into 4 groups: sham operation group, ischemia control group, ischemia plus VEGF intraperitoneal injection group, ischemia and EPCs transplantation group and MCAO group. At 3, 7, 14, 30 and 60 days, the vascular densities of cerebral ischemia and peripheral regions in each group and the electrophysiological indexes (somatosensory evoked potential and motor evoked potential) and behavioral changes (sensory injury transference test, Motor Function Test and mNSS Modified Neurological Function Score). Results Compared with ischemic control group (P <0.05), the neovascularization density in the group of ischemia plus VEGF intraperitoneal injection and ischemia and EPCs transplantation group were higher than those in the ischemic control group at all other time points (P <0.05) The density of neovascularization in the cloned antibody group was lower than that in the ischemic control group at the last 5 time points (P <0.05). The levels of somatosensory evoked potentials and motor evoked potentials were significantly different from the ischemic control group after 7 days in ischemic group, intraperitoneal injection of VEGF, ischemia and EPCs transplantation, and MCAO plus ischemia / reperfusion (P <0.05). Compared with ischemic control group, there was a significant difference in behavioral score after 3 days between Ischemia plus intraperitoneal injection of VEGF, Ischemic + EPCs and Ischemic plus vascular endothelial factor monoclonal antibody group (P < 0.05). Conclusion Exogenous intervention of ischemic angiogenesis in rat model of cerebral ischemia can affect the repair of neurological deficits. The same effect can be achieved by single injection of vascular endothelial progenitor cells and multiple injections of VEGF.