血管紧张素Ⅱ促进血管平滑肌细胞Lox-1 mRNA表达  

Effect of angiotensin Ⅱ on Lox-1 m RNA expression through vascular smooth muscles cells

作　　者：魏钧伯[1] 黄冬[1] 马健[1] 魏盟[1] 陆志刚[1] 马士新[1] 蔡迺绳[2] 

机构地区：[1]上海交通大学附属上海市第六人民医院心内科,上海200233 [2]上海复旦大学附属中山医院心内科,上海200032

出　　处：《世界临床药物》2014年第12期724-726,共3页World Clinical Drug

摘　　要：目的观察血管紧张素Ⅱ(AngⅡ)对血管平滑肌细胞(VSMC)凝集素样氧化低密度脂蛋白受体-1(Lox-1)表达的影响。方法人脐带动脉平滑肌细胞体外原代培养。AngⅡ干预,RT-PCR测定VSMC Lox-1 m RNA表达,并观察AngⅡ受体1(AT1R)阻断剂氯沙坦和AngⅡ受体2(AT2R)阻断剂PD123319对AngⅡ上述作用的影响。结果 AngⅡ作用于VSMC后,Lox-1 m RNA表达增强(P<0.001)。氯沙坦阻断AT1R后,Lox-1 m RNA表达显著下降(P<0.001)。PD123319阻断AT2R后,Lox-1 m RNA表达无明显变化。结论 AngⅡ明显促进VSMC Lox-1 m RNA表达,在此过程中AT1R的介导作用更为显著。objective To observe the effect of Ang Ⅱ on Lox-1 mRNA expression through VSMC. Methods Smooth muscle cell from human umbilical artery was cultured in vitro. The interaction with Ang Ⅱ and the detection of VSMC Lox- 1 mRNA quantity with RT-PCR were performed. Furthermore, the impact of Losartan （AT 1 R） and PD 123319 （AT2R） on the effect ofAng Ⅱ were observed. Results The quantity of VSMC Lox-1 mRNA was obviously increased after cocultured with Ang Ⅱ （P〈0.001）. The quantity ofVSMC Lox-1 mRNA was decreased significantly after AT1R was blocked by Losartan （P〈 0.001）. There is no obvious change of VSMC Lox- 1 mRNA expression after AT2R blocked by PD 123319. Conclusion Ang Ⅱ can induce increased expression ofVSMC Lox-1 mRNA. AT1R plays a key role in this process.

关 键 词：动脉粥样硬化 血管紧张素Ⅱ 凝集素样氧化低密度脂蛋白受体-1 

分 类 号：R541.4[医药卫生—心血管疾病]