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血管紧张素ⅡⅠ型受体反义寡核苷酸逆转心肌成纤维细胞增殖及胶原合成的实验研究(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2004年第2期
页码:
99-102
栏目:
基础研究
出版日期:
2004-03-01

文章信息/Info

Title:
Investigation of angiotensinⅡ typeⅠ receptor antisense oligonucleotide on reversing proliferation and collagen synthesis of cardiac fibroblasts
作者:
孙琦; 王晋明; 王颖; 王晶; 胡萍; 胡文兰; 牛萍
武汉大学人民医院心内科,湖北 武汉 430060
Author(s):
SUN Qi; WANG Jin-ming; WANG Ying; WANG Jing; HU Ping; HU Wen-lan; NIU Ping
Department of Cardiology, Renmin Hospital, Wuhan University, Wuhan, Hubei 430060, China
关键词:
心肌成纤维细胞; AT1R-AS-ODN; 血管紧张素Ⅱ; c-jun基因
Keywords:
cardiac fibroblasts;  Ang;  AT1R-AS-ODN;  c-jun gene
分类号:
R542.2
DOI:
-
文献标识码:
A
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)体外逆转心肌成纤维细胞增殖及胶原合成。方法:将培养的乳鼠心肌成纤维细胞分为正常组、AngⅡ组、AT1R-AS-ODN组,观察AngⅡ及AT1RAS-ODN对心肌成纤维细胞c-jun基因表达、成纤维细胞增殖、3H-Proline掺入率的影响。结果:AngⅡ可刺激心肌成纤维细胞增殖、c-jun基因表达增多、3H-Proline掺入率增加。AT1R-AS-ODN能逆转AngⅡ的上述作用。结论:AT1R-AS-ODN能有效逆转AngⅡ诱导的心肌成纤维细胞增殖及胶原合成。
Abstract:
AIM:To study angiotensinⅡ typeⅠ receptor antisense oliagonucleotide (AT1R-ASODN) reversing proliferation and collagen synthesis of cardiac fibroblasts. METHODS: The cultured neonatal rat cardiac fibroblasts were divided into 3 groups: AngⅡ group (10-6mol/L AngⅡ), AT1R-AS-ODN treatment group (10-6mol/LAngⅡ+AT1R-AS-ODN) and control group. To investigate the effects of AngⅡ and AT1R-AS-ODN onc-jun gen expression,proliferation and 3H-Proline in corporation of cardiac fibroblasts. RESULTS: C-jun protein O.D. amountofAngⅡ groupincreasedto0.26± 0.11,butinAT1R-AS-ODN treatment group decreased to 0.23±0.08; The cell density of AngⅡ group increased to (260.7±17.9)×104/ml, but decreased to 116.8± 11.4)× 104/ml in AT1R-AS-ODN treatment. And 3H-Proline in corporation in creased to 294.3±19.8 cpm in AngⅡ group, but decreased to 234.6±25.4 cpm in AT1R-AS-ODN treatment group. CONCLUSION: AT1R-AS-ODN can reverse the increase of c-jun gene expression, proliferation and 3H-Proline in corporation of cardiac fibroblasts induced by AngⅡ.

参考文献/References

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备注/Memo

备注/Memo:
收稿日期：2003-5-26
更新日期/Last Update: 2004-03-01