中文摘要：

目的：观察黄芪多糖对缺氧再复氧损伤的人心脏微血管内皮细胞细胞间黏附分子-1（ICAM-1）和血管细胞黏附分子-1（VCAM-1）蛋白表达的影响。方法：以体外缺氧缺糖模拟体内缺血,复氧复糖模拟再灌注复制缺血再灌注损伤模型;采用免疫细胞化学法和图象定量分析系统观察ICAM-1、VCAM-1蛋白表达的变化。结果：人心脏微血管内皮细胞复苏48-72h后呈铺路石样生长,在15个细胞倍增周期内,其形态、生物、生理学特性稳定。与正常对照组比较,缺氧再复氧可明显增加ICAM-1、VCAM-1蛋白在人心脏微血管内皮细胞的表达（P〈0.01）。黄芪多糖能降低两者的表达,其中100μg/mL抑制ICAM-1表达的作用显著（P〈0.05）,100、50μg/mL减少VCAM-1表达的作用明显（P〈0.01）。结论：黄芪多糖通过减少缺血再灌注损伤的人心脏微血管内皮细胞ICAM-1和VCAM-1的表达,抑制白细胞的浸润,从而减轻心肌缺血再灌注损伤。

英文摘要：

Objectives： To observe effect of astragalus polysaccharides（APS） on the protein expression of intercellular adhesion molecule - 1 （ ICAM - 1 ） and vascular cell adhesion molecule - 1 （ VCAM - 1 ） in human cardiac microvaseular endothelial cells（HCMEC） injury induced by Hypoxia and Reoxygenation. Methods： Ischemia and reperfusion injury model was established by oxygen - glucose deprivation and recovery method in vitro. Protein expression of ICAM - 1 and VCAM - 1 was determined by immunocytochemistry and image quantitative analysis system. Results： The HCMEC showed a typical cobblestone appearance after recovered for 48h - 72h and it＇s characters of morphology, biology and physiology were stabilization during the 15 population dou- bling periods. Compared with control group, the expression of ICAM - 1 and VCAM - 1 of HCMEC after hypoxia and reoxygenated were increased obviously（ P 〈 0.01 ）. 100μg,/mL of APS could significantly inhibit the expression of ICAM - 1 （ P 〈 0.05 ）, and 100μg/mL,50μg/mL of APS could evidently decrease the expression of VCAM - 1 （ P 〈 0.01 ）, compared with model group. Conclusion ： APS could alleviate the mocardial repeffusion injury. Its mechanism might be related with reducing expression of ICAM - 1 and VCAM - 1 in HCMEC, inhibiting leukocytes infiltration.