血管紧张素ⅡⅠ型受体反义寡核苷酸体外逆转心肌细胞肥大  

Investigation on AngiotensinⅡTypeⅠReceptor AntisenseOligonucleotide in Reversing Cardiac Myocytes Hypertrophy

作　　者：孙琦[1] 王晋明[2] 王颖[2] 王晶[2] 胡萍[2] 胡文兰[2] 牛萍[2] 

机构地区：[1]安徽省立医院心内科,合肥230001 [2]武汉大学人民医院心内科,武汉430060

出　　处：《武汉大学学报（医学版）》2005年第2期183-185,189,共4页Medical Journal of Wuhan University

基　　金：湖北省教育厅自然基金资助项目(编号:301140080)

摘　　要：目的:用血管紧张素Ⅱ(AngⅡ)Ⅰ型受体(AT1R)反义寡核苷酸(AS ODN)逆转心肌细胞肥大。方法:将培养的乳鼠心肌细胞分为正常组、AngⅡ组、AT1R AS ODN组,观察AngⅡ及AT1R AS ODN对心肌细胞 c jun基因表达、总蛋白合成、体积、搏动频率的影响。结果:AngⅡ可引起心肌细胞 c jun基因表达增多、搏动频率增快、体积增大、总蛋白合成增加。AT1R AS ODN能逆转 AngⅡ的上述作用。结论:AT1R AS ODN能有效逆转 AngⅡ诱导的心肌细胞肥大。Objective: To study the function of angiotensin(Ang)ⅡtypeⅠreceptor antisense oligonucleotide(AT_1R-AS-ODN) in reversing cardiac myocytes hypertrophy. Methods: The cultured neonatal rat cardiac myocytes were divided into 3 groups: AngⅡ group(10 -6 mol·L -1 AngⅡ),AT_1R-AS-ODN treatmeat group(10 -6 mol·L -1 AngⅡ+ AT_1R-AS-ODN) and control group. To investigate the effects of AngⅡ and AT_1R-AS-ODN on c-jun gene expression, total protein synthesis, volum and beat frequency of cardiac myocytes were measured. Results: The c-jun protein OD value of cardiac myocytes in AngⅡ group increased to 0.25±0.05,but decreased to 0.21±0.07 in AT_1R-AS-ODN treatmeat group. In AngⅡ group, total protein synthesis of cardiac myocytes increased to (10.78±0.34) mg·ml -1 ,but decreased to (8.9±0.56) mg·ml -1 in AT_1R-AS-ODN treatmeat group. In AngⅡ group, diameter of cardiac myocytes increased to (17.65±2.81)μm ,but decreased to (11.94±2.12)μm in AT_1R-AS-ODN treatmeat group. And beat frequency of cardiac myocytes increased to (66±3) times per minute in AngⅡ group, while decreased to (50±2) times per minute in AT_1R-AS-ODN treatmeat group. Conclusion: AT_1R-AS-ODN can reverse the increase of c-jun gene expression, total protein synthesis, volum and beat frequency of cardiac myocytes induced by AngⅡ.

关 键 词：心肌细胞 心肌细胞肥大 血管紧张素Ⅱ AT1R-AS-ODN C-JUN基因 

分 类 号：R544.1[医药卫生—心血管疾病]