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

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.