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目的探讨脑缺血再灌注大鼠不同时间碱性成纤维细胞生长因子(bFGF)和血小板源性生长因子-B(PDGF-B)的表达水平及其与血管形成的关系。方法采用线栓法制备大鼠大脑中动脉局灶性脑缺血再灌注(MCAO/R)模型,分为假手术组和MCAO/R组,MCAO/R组缺血2 h后根据再灌注时间窗的不同分为0、6、24 h、3、7、14、21 d共7组,应用HE染色观察病理变化并测定脑梗死体积,用免疫组化法检测CD34蛋白的表达水平并计数微血管密度(MVD),用免疫组化法检测bFGF和PDGF-B蛋白的表达水平。结果 bFGF蛋白表达水平在MCAO/R6 h后即开始升高,3 d到达高峰,7 d开始降低。PDGF-B蛋白表达水平在MCAO/R24 h后明显升高,3 d到达高峰,7 d有所下降,持续到14 d左右。MVD表达在MCAO/R3 d开始升高,7 d到达高峰。bFGF和PDGF-B蛋白表达水平与MVD变化呈正相关(P<0.01)。结论局灶性脑缺血再灌注损伤可诱导bFGF、PDGF-B和新生血管表达增加,激活内源性脑保护机制。
Objective To investigate the expression of basic fibroblast growth factor (bFGF), platelet derived growth factor-B (PDGF-B) and their relationship with angiogenesis in rats with cerebral ischemia-reperfusion. Methods The focal middle cerebral artery occlusion (MCAO / R) model of middle cerebral artery (MCAO / R) was established by thread occlusion in rats. The model was divided into sham operation group and MCAO / R group. MCAO / R group was divided into two groups according to reperfusion time The windows were divided into 7 groups at 0, 6, 24 h, 3, 7, 14 and 21 days. The pathological changes were observed by HE staining and the volume of cerebral infarction was measured. The expression of CD34 protein was detected by immunohistochemistry and counted for microvessel Density (MVD), the expression of bFGF and PDGF-B protein were detected by immunohistochemistry. Results The expression of bFGF began to increase after MCAO / R6 h, peaked at 3 d, and decreased at 7 d. The level of PDGF-B protein increased significantly after MCAO / R24h, peaked on the third day, and decreased on the seventh day, lasting for about 14 days. MVD expression began to increase at MCAO / R3d and peaked at 7d. The expressions of bFGF and PDGF-B were positively correlated with MVD (P <0.01). Conclusion Focal cerebral ischemia-reperfusion injury can induce the expression of bFGF, PDGF-B and neovascularization to increase and activate the endogenous brain protection mechanism.