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目的 探讨局灶性脑缺血再灌注后血管内皮生长因子 (VEGF)蛋白表达的意义及地塞米松对其影响。 方法 采用老年雄性大鼠短暂性大脑中动脉闭塞 (MCAO)与再灌注模型 ,应用免疫组织化学方法观察大脑中动脉闭塞 90min再灌注 1～ 7d脑组织VEGF蛋白的表达及腹腔内注射地塞米松 ( 2mg·kg-1 ·d-1 ,持续 7d)对VEGF蛋白表达及脑组织含水量的影响。 结果 实验大鼠再灌注1h ,缺血半暗带神经元及同侧大脑中动脉供血区软脑膜开始表达VEGF ,1d达峰值 (P <0 0 1) ,前者于 1d后快速下降 ,后者维持高水平至 7d。缺血半暗带脑血管内皮细胞在 1～ 7d也有较丰富VEGF表达 (P <0 0 1)。地塞米松处理组缺血区的脑微血管内皮细胞VEGF表达明显减少 (P <0 0 1)。地塞米松在缺血再灌注 1～ 7d明显减少缺血脑组织含水量 (P <0 0 5)。 结论 局灶性脑缺血再灌注可诱导VEGF表达 ,地塞米松可抑制缺血再灌注脑组织血管内皮细胞VEGF表达
Objective To investigate the significance of vascular endothelial growth factor (VEGF) protein expression after focal cerebral ischemia-reperfusion and the effect of dexamethasone on it. Methods The transient middle cerebral artery occlusion (MCAO) and reperfusion model of aged male rats were used to observe the expression of VEGF protein in brain tissue of middle cerebral artery occlusion 90min after reperfusion and the expression of VEGF in intraperitoneal injection of dexamethasone 2mg · kg-1 · d-1 for 7 days) on VEGF protein expression and brain water content. Results After 1h of reperfusion, the expression of VEGF in ischemic penumbra neurons and ipsilateral middle cerebral artery began to reach peak at 1d (P <0.01). The former decreased rapidly after 1d and the latter maintained High level to 7d. Cerebral vascular endothelial cells in ischemic penumbra also had more abundant VEGF expression from 1 to 7 days (P <0.01). Dexamethasone treatment group ischemic brain microvascular endothelial cell VEGF expression was significantly reduced (P lt; 0 0 1). Dexamethasone markedly decreased the water content of ischemic brain tissue at 1 ~ 7d after ischemia / reperfusion (P <0.05). Conclusion Focal cerebral ischemia-reperfusion can induce VEGF expression. Dexamethasone can inhibit VEGF expression of vascular endothelial cells in ischemia-reperfusion brain tissue