血管内皮生长因子和碱性成纤维细胞生长因子在缺血预处理大鼠局灶性脑缺血再灌注区域的表达

背景：脑缺血预处理可增加碱性成纤维细胞生长因子的表达，可能导致脑缺血耐受的产生。大鼠大脑中动脉缺血再灌注给予血管内皮生长因子能够起到神经保护作用。 目的：观察缺血预处理对缺血再灌注大鼠血管内皮生长因子和碱性成纤维细胞生长因子表达的影响。 方法：将SD大鼠随机分为缺血预处理组、模型组和假手术组。缺血预处理及模型组线栓法阻塞大脑中动脉制备脑缺血模型。预处理组在脑缺血-再灌注前3 d用插入尼龙线阻塞大脑中动脉，缺血2 h后再灌注22 h。模型组第一次手术将线栓前推5 mm，不阻断血流，其他同预处理组。假手术组仅插入尼龙线不阻塞大脑中动脉。用苏木精-伊红染色法观察3组间神经细胞变化。用抗生物素-生物素-过氧化物酶复合物法检测各组血管内皮生长因子和碱性成纤维细胞生长因子蛋白的表达。分别比较3组神经功能评分、光镜下脑缺血再灌注区神经细胞形态、血管内皮生长因子和碱性成纤维细胞生长因子的表达。 结果与结论：与模型组比较，预处理组神经功能评分明显低于模型组(P < 0.01)。光镜下观察结果显示，与模型组比较，预处理组缺血面积及缺血程度均减轻，血管内皮生长因子和碱性成纤维细胞生长因子表达均明显升高(P < 0.05)。结果提示缺血预处理可能通过增强血管内皮生长因子和碱性成纤维细胞生长因子而对缺血再灌注大鼠神经细胞起保护作用。

Expression of vascular endothelial growth factor and basic fibroblast growth factor in rat focal cerebral ischemia reperfusion region following ischemic preconditioning

BACKGROUND: Cerebral ischemic preconditioning (IPC) can increase basic fibroblast growth factor (bFGF) expression, which may induce brain ischemic tolerance. Injection of vascular endothelial growth factor (VEGF) into cerebral ischemia/reperfusion region can play neuroprotective effect. OBJECTIVE: To observe the effect of focal ischemic preconditioning on VEGF and bFGF expression in rat with cerebral ischemia reperfusion. METHODS: Sprague Dawley rats were randomly divided into 3 groups. Middle cerebral artery occlusion (MCAO) and ischemic preconditioning model rats were established by thread ligation. The IPC group received IPC at 3 days and 2 hours of MCAO and rats were killed after 22 hours reperfusion; model group did not receive IPC; the control group received sham surgery two times. Nerve cell changes in the 3 groups were observed by haematoxylin-eosin staining. The expression of VEGF and bFGF protein was determined by avidin biotin-peroxidase complex method. Neurologic score and cerebral cortex changes and immunohistochemistry of VEGF and bFGF were compared in each group. RESULTS AND CONCLUSION: Compared with the model group, the neurological deficit scores of the IPC group were obviously smaller (P < 0.01), the ischemia area and degree were lessened, but the expression of VEGF and bFGF were evidently increased (P < 0.05). Focal cerebral ischemic preconditioning can induce ischemic neuroprotective effect and its mechanism may be related with the expression of VEGF and bFGF.