氧化低密度脂蛋白通过激活内皮细胞受体诱发一氧化氮的产生  

Oxidized low density lipoprotein stimulated endothelial nitric oxide by activating lectin like oxidized LDL receptor

作　　者：徐雅琴[1] 张钧华[1] 柯杨[2] 曹静[1] 宁涛[2] 冯利雅[2] 唐朝枢[1] 

机构地区：[1]北京大学第一医院心血管病研究所,北京100034 [2]北京大学临床肿瘤学院,北京100034

出　　处：《北京大学学报（医学版）》2001年第2期150-152,共3页Journal of Peking University:Health Sciences

摘　　要：目的 :探讨氧化低密度脂蛋白内皮受体LOX1在氧化低密度脂蛋白 (oxidizedlowdensitylipoprotein ,ox LDL)对内皮细胞产生一氧化氮 (nitricoxide,NO)影响中的作用。方法 :反转录聚合酶链反应 (RT PCR)检测LOX1mRNA的表达 ,酶法检测NO含量。结果 :ox LDL可上调内皮细胞LOX1mRNA的表达 ,同时诱发内皮细胞产生NO ,且呈浓度依赖效应 ,应用LOX1抑制剂可抑制这一作用。结论 :ox LDL可诱发内皮细胞NO的产生 ,呈浓度依赖效应 。SUMMARY Objective:To explore the role of lectin like oxidized low density lipoprotein (ox LDL) receptor(LOX1) in ox LDL stimulating endothelial nitric oxide(NO) production. Methods: LOX1 mRNA expression was detected by reverse transcription polymerase chain reaction(RT PCR). The quantity of NO was detected by Enzyme method. Results: Incubation of ox LDL increased endothelial NO production and LOX1 mRNA expression. When HUVECs were incubated with ox LDL as well as the inhibitor of LOX1, polyinosinic acid,the increase of NO production and LOX1mRNA expression were attenuated. Conclusion: Ox LDL enhanced endothelial NO production in a concentration dependent manner, and the effect of ox LDL on endothelial NO was mediated by LOX1.

关 键 词：氧化低密度脂蛋白 内皮细胞受体 一氧化氮 动脉硬化 

分 类 号：Q513.5[生物学—生物化学] R543.5[医药卫生—心血管疾病]