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机构地区:[1]华中科技大学同济医学院附属协和医院老年病科,武汉430022
出 处:《华中科技大学学报(医学版)》2008年第4期453-456,共4页Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
摘 要: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。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 umbilical vein endothelial cells. Methods The levels of NO, ICAM-1 and NOS were determined by nitrate reductase method, cell ELISA method, immunohistochemical and image analysis method, respectively. Results The ox-LDL could significantly increase the expression of ICAM-1 and inhibit the expression of NO and NOS in a dose-dependent manner. Fosinopril and valsartan could significantly inhibit those roles of ox-LDL. The roles of fosinopril and valsartan had no difference. Conclusion Fosinopril and valsartan can inhibit ox-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 their antiatherosclerosis.
关 键 词:福辛普利 缬沙坦 动脉粥样硬化 细胞间黏附分子-1 一氧化氮
分 类 号:R543.5[医药卫生—心血管疾病]
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