福辛普利与缬沙坦对氧化型低密度脂蛋白诱导的人脐静脉内皮细胞ICAM-1及NO表达的影响

目的研究福辛普利与缬沙坦对氧化性低密度脂蛋白(oxidized low density lipoprotein,ox-LDL)诱导的脐静脉内皮细胞细胞间黏附分子-1(intercellul aradhesion molecule-1,ICAM-1)及一氧化氮(nitric oxide,NO)表达的影响。方法采用硝酸还原酶法测定细胞培养液上清中NO的含量,细胞ELISA法测定细胞表面ICAM-1的含量,免疫组织化学法结合图像分析测定细胞一氧化氮合酶(nitric oxide synthase,NOS)含量。结果ox-LDL可明显增加脐静脉内皮细胞各时点ICAM-1的表达,并减少NO及NOS的表达,且有浓度依赖性。福辛普利与缬沙坦均可显著抑制ox-LDL的上述作用,两者作用的差异无显著性意义。结论抑制ox-LDL诱导的内皮细胞ICAM-1的表达,并增加内皮细胞NO的合成,可能为福辛普利与缬沙坦抗动脉粥样硬化的作用机制之一。

Effects of fosinopril and valsartan on expressions of ICAM-1 and NO in human umbilical vein endothelial cells

Objective To investigate the effects of fosinopril and valsartan on the expression of intercellular adhesion molecule-1 (ICAM-1) and nitric oxide (NO) induced by oxidized low-density lipoprotein (ox-LDL) in human umbilical vein endothelial cells.Methods The levels of NO, ICAM-1, and nitric oxide synthase (NOS) were determined using the nitrate reductase method, ELISA, immunohistochemical and image analyses.Results The ox-LDL can significantly increase the expression of ICAM-1 and inhibit the expression of NO and NOS in a dose-dependent manner. Fosinopril and valsartan can significantly inhibit these roles of ox-LDL. The roles of fosinopril and valsartan were not significantly different.Conclusion Fosinopril and valsartan inhibit oxidized LDL-induced expression of ICAM-1 and increase the expression of NO in human umbilical vein endothelial cells, which is one of the mechanisms of antiatherosclerosis.