中文摘要：

目的 探讨糖基化终产物（AGEs）与其受体（RAGE）对ECV-304细胞上血管细胞黏附分子-1（ICAM-1）和细胞间黏附分子-1（VCAM-1）的影响,为研究AGEs在动脉粥样硬化发生发展中的作用提供实验依据.方法 采用体外制备的糖基化终产物——糖基化的牛血清白蛋白（AGE-BSA）和反义RAGE寡核苷酸处理ECV-304细胞,通过流式细胞仪技术、Western印迹技术检测ECV-304细胞上ICAM-1、VCAM-1蛋白质的表达.结果 AGEs处理ECV-304细胞后,可诱导ECV-304细胞上VCAM-1和ICAM-1的表达增加,且这种效应呈剂量依赖性.采用反义技术阻断RAGE的mRNA水平的翻译后,ECV-304细胞ICAM-1和VCAM-1的表达呈剂量依赖性降低.结论 AGEs可通过与其膜受体RAGE的结合激活血管内皮细胞VCAM-1和ICAM-1的表达,这可能是AGEs促动脉粥样硬化发生发展的机制之一.

英文摘要：

Objective To explore the role of advanced glycation end products （AGEs） and it＇s receptor （RAGEs） in modulating the expression of intercellular adhesion molecule-1 （ICAM-1 ） and vascular cell adhesion molecule-1 （VCAM-1） in human ECV-304 cell line. Methods Human ECs （ECV-304 cell line） were cultured in RPMI （Gibco -BRL） supplemented with 10% FCS （HyClone）. AGEs was prepared by incubating 30% bovine serum albumin （BSA） with 16% glucose for 60 days at 37℃. Antisense technique was used to investigate the role of RAGE on the effect of AGEs in the endothelial cells. The expression of ICAM-1 and VCAM-1 was detected by flow cytometry and western blotting . Results Human ECs expressed ICAM-1 and VCAM-1. Treatment of ECs with the AGEs increased the expression of ICAM-1 and VCAM-1 protein in vitro in a concentration-dependent manner. But the effect was blocked by antisense RAGE oligonueleotides in a concentration- dependent manner. Conclusion AGEs may has proatherosclerotic potential by modulating the expression of ICAM-1 and VCAM-1 in ECV-304 cells, RAGE also participates the process. The study may provide a mechanism for pathogenesis of atherosclerosis induced by diabetes mellitus.