中文摘要：

目的探讨在糖尿病大鼠的视网膜组织中，视网膜血管内皮生长因子（VEGF）通过激活蛋白激酶C（PKC），上调一氧化氮（N0）含量，促使细胞间黏附因子-1（ICAM-1）升高的信号机制。方法腹腔注射链脲佐菌素（STZ）建立糖尿病大鼠模型。设立正常组、糖尿病组、糖尿病大鼠PKC抑制剂组、二甲基亚砜对照组。应用硝酸还原酶法检测视网膜组织中N0含量，应用Western-blot检测VEGF及ICAM-1蛋白含量。结果在糖尿病大鼠视网膜中VEGF、NO含量较正常大鼠明显升高（P〈0．05）。应用PKC抑制剂24h，视网膜组织中VEGF、NO含量明显下降，与二甲基亚砜对照组相比有显著差异（P〈0．05）。ICAM-1含量也呈现出相应的变化趋势，糖尿病大鼠视网膜中的ICAM-1较正常大鼠显著增高（P〈0．01）。而应用PKC抑制剂24h，ICAM-1的表达明显低于二甲基亚砜对照组（P〈0．01）。VEGF、NO、ICAM-1的含量在二甲基亚砜对照组与糖尿病组之间的差异无统计学意义。结论链脲佐菌素诱导的糖尿病大鼠视网膜病变中ICAM-1蛋白表达升高，可能是通过VEGF／PKC／NO这一信号通路完成的。

英文摘要：

Objective To investigate how vascular endothelial growth factor （VEGF） up-regulates intercellular adhesion molecule-1 via protein kinase C （PKC）/ nitric oxide （NO） pathway in the retina of diabetic rats. Methods All the rats were divided into 4 groups： normal, diabetes, diabetes＋ PKCI and control groups. Diabetes was induced by an intraperitoneal injection of STZ. PKC inhibitor GF109203X was injected intravitreaUy after 5 months of streptozotocin induced diabetes. NO was determined by nitrate reductase method. VEGF and intercellular adhesion molecule-1 （ICAM-1） were measured by Western blot. Results VEGF and NO expressions increased obviously in the retina of diabetic rats compared with those in the normal group （P〈 0.05）. So was ICAM-1 expression （P〈0.01）. VEGF and NO expressions decreased significantly 24 hours after GF109203X was injected compared with those in the control group （P〈0.05）. So was ICAM-1 expression （P〈0.01）. However, no significant differences were found in VEGF, NO or ICAM-1 expressions between the diabetic group and the control group. Conclusion The results suggest that ICAM-1 might be up-regulated by VEGF via PKC/NO pathway in diabetic retinopathy in rats.