【摘要】 为探讨血管紧张素转化酶抑制剂拉米普利酸对氧化型低密度脂蛋白损伤血管内皮细胞是否具有保护作用，采用反转录多聚酶链反应技术来观察拉米普利酸对氧化型低密度脂蛋白诱导培养的人脐静脉内皮细胞ｃ－ｍｙｃｍＲＮＡ的影响，并用Ｇｒｉｅｓｓ法和放射免疫法分别测定拉米普利殴作用前后培养的脐静脉内在细胞一氧化氨和ｃＧＭＰ的含量。结果发现，氧化型低密度脂蛋白促进人脐静脉内皮细胞ｃ－ｍｙｃ表达（Ｐ＜０．０５），明显降低一氧化氨和ｃＧＭＰ含量（Ｐ＜０．０５）。拉米普利酸对氧化型低密度脂蛋白诱导内皮细胞：ｃ－ｍｙｃ表达具有抑制作用，并能增加一氧化氨和ｃＧＭＰ水平。拉米普利酸的效应可被一氧化氮合成酶抑制剂硝基－左旋精氨酸部分取消。此结果提示拉米普利酸可促进一氧化氮释放而抑制氧化型低密度脂蛋白诱导内皮细胞ｃ－ｍｙｃ过度表达。更多还原

【Abstract】 ABSTRACTAim To investigate the effects and mechanism oframiprilat on c-myc expression induced by oxidized lowdensity lipoprotein (x-LDL) in vascular endothelialcells.Method After endothelial cells incubated with ox-LDL (250 mg/L) , ox-LDL+ramiprilat (20 mol/L) ,ox-LDL+ ramiprilat (40 mol/L) + N-Arg (1 00 mol/L ) , ox-LDL+N-Arg for 4 h in vitro. Reverse tran-scription PCR technique was employed to measure c-myc mRNA of cultured human umbilical vein endothe-lial cells (HUVEC). Nitric oxide (NO) and cGMPwere assayed by means of Griess reaction and radioim-munoassy respectively.Results in response to ox-LDL (250 mg/L) for 4 h,c-myc mRNA transcription of endothelial cells signifi-cantly increase (P<0. 05). In contrast , NO releaseand cGMP contents markedly decreased (P< 0. 05).Ramiprilat ( 20, 40 mol/L ) inhibited ox-LDL-in-duced c-myc expression and increased NO ,cGMP levelsof HUVEC. The effects of ramiprilat was partlyabolished by nitro-L-Arginine, a compeptitive in-hibitor of NO synthetase.Conclution Ramiprilat suppresses OLDL-induced c-myc overexpresion of endothelial cells by enhencingNO release.KEY WORDS Ramiprilat ; Low density lipopro-tein : Endothelial cell ; c-myc i Nitric oxide ;cGMP更多还原