AIM： To explore the relationship between intercellular adhesionmolecule-1(ICAM-1)expression in endothelial cells(EC) and advanced glycosylation end products(AGEs) stimulation. METHODS: Murine bone marrow derived ECs was stimulated by AGEs after pretreated with anti-AGEs, anti-IL-1β and N-acetylcysteine(NAC),then SOD activity and ICAM-1 concentration and adhesion rate(AR) were evaluated. RESULTS: ECs which expressed ICAM-1[(0.65±0.14） vs （0.11±0.02）] induced by AGEs showed lower SOD activity [(0.69±0.19）×103 U/L vs （1.71±0.42）×103 U/L]. The ICAM-1 expression as well as the increase of AR caused by AGEs stimulation could be suppressed by anti-AGEs(0.12±0.01） and NAC(0.11±0.05）. Anti-IL-1β had no influence on these changes. CONCLUSION： AGEs could induce endothelial cells to express ICAM-1 in vitro, most probably due to the formation of free radicals. Besides, AGEs may stimulate other cells to secrete cytokines resulting in ICAM-1 expression in endothelial cells.%目的：探讨糖基化终产物(AGEs)致内皮细胞表达细胞间粘附分子-1(ICAM-1)与自由基产生之间的关系。方法：内皮细胞(EC)用抗AGEs抗体、抗IL-1β多抗、N-乙酰半胱氨酸(NAC)预处理1h后AGEs作用6h，测定IL-1β、超氧化物歧化酶(SOD)、ICAM-1、内皮细胞-中性粒细胞粘附率。结果：AGEs刺激后ICAM-1表达增加[吸光度(A)为0.65±0.14vs0.11±0.02]的内皮细胞SOD活性降低[(0.69±0.19）×103U/Lvs（1.71±0.42）×103U/L]。ICAM-1的增加可被抗AGEs抗体[吸光度(A)为(0.12±0.01）]、NAC[吸光度(A)为(0.11±0.05）]和抗ICAM-1抗体[吸光度(A)为(0.10±0.04）]抑制。外源性IL-1β也可刺激内皮细胞表达ICAM-1[吸光度(A)为(0.72±0.23）]。结论：AGEs刺激内皮细胞表达ICAM-1可能与其导致细胞自由基的产生有关；AGEs还可通过刺激其他细胞产生细胞因子间接作用于EC，参与促进ICAM-1表达。
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