中文摘要：

目的：探讨磷脂酰肌醇-3激酶（phosphatidylinositol 3-kinase，PI3K）信号转导通路对缺氧诱导的视网膜色素上皮（retinal pigment epithelium，RPE）细胞表达VEGF的影响。 方法：利用CoCl2建立培养的人RPE细胞缺氧模型，分为单纯缺氧组和30μmol/L PI3K特异性阻断剂LY294002阻断处理组，在缺氧条件下分别培养0，1，4，8，12和24h.细胞免疫荧光法检测磷酸化PI3K表达水平；酶联免疫吸附试验（enzyme linked immunosorbent assay，ELISA）检测RPE细胞上清中VEGF的含量。 结果：缺氧刺激1，4，8，12和24h，RPE细胞膜上PI3K磷酸化表达水平逐渐增高（P＜0.05）；随缺氧时间延长，RPE细胞上清液中VEGF含量逐渐增加（P＜0.05）；LY294002处理组VEGF含量显著低于对照组（P＜0.05）。 结论：PI3K信号转导通路参与了缺氧引起的人RPE细胞VEGF表达的调控。

英文摘要：

AIM： To investigate the role of phosphatidylinositol 3-kinase （PI3K）signal transduction pathway in vascular endothelial growth factor（VEGF）expression in cultured human retinal pigment epithelial（RPE） cells under hypoxia. METHODS： Cobalt chloride was used to establish a model of hypoxia and RPE cells treated with/without the specific inhibitor of PI3K, LY294002 at the concentration of 30μmol/L. The level of phosphophorylation PI3K was observed with immunofluorescence staining. The amounts of VEGF in the RPE-conditioned supernatant were measured using enzyme linked immunosorbent assay. RESULTS： Under hypoxia, the level of PI3K phosphophory-lation in RPE cells was time-dependently increased in cell membrane （P〈0.05）. The amount of VEGF in RPE cell supernatant was significantly increased in time-dependent manner under hypoxia （P〈0.05）, and that in LY294002-treatecl groups was lower than the controls （P〈0.05）. CONCLUSION： PI3K signal transduction pathway could partly play a positive role in VEGF expression induced by hypoxia in RPE cells.