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作 者:孙琦[1] 王晋明[1] 王颖[1] 王晶[1] 胡萍[1] 胡文兰[1] 牛萍[1]
机构地区:[1]武汉大学人民医院心内科,湖北武汉430060
出 处:《心脏杂志》2004年第2期99-102,共4页Chinese Heart Journal
基 金:湖北省教育厅自然基金资助 (文号 /项目编号 :2 0 0 0 B0 3 0 2 3 /3 0 114 0 0 80 )
摘 要:目的 :用血管紧张素 (Ang ) 型受体 (AT1 R)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、Ang 组、AT1 R- AS- ODN组 ,观察 Ang 及 AT1 R-AS- 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 :Ang 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。 AT1 R- AS- ODN能逆转 Ang 的上述作用。结论 :AT1 R- AS- ODN能有效逆转 Ang 诱导的心肌成纤维细胞增殖及胶原合成。AIM:To study angiotensinⅡ typeⅠ receptor antisense oliagonucleotide(AT 1R-AS-ODN) 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),AT 1R-AS-ODN treatment group (10 -6mol/L AngⅡ+AT 1R-AS-ODN) and control group. To investigate the effects of AngⅡ and AT 1R-AS-ODN on c-jun gene expression,proliferation and 3H-Proline incorporation of cardiac fibroblasts. RESULTS:C-jun protein O.D.amount of AngⅡ group increased to 0.26±0.11,but in AT 1R-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 AT 1R-AS-ODN treatment. And 3H-Proline incorporation increased to 294.3±19.8 cpm in AngⅡ group,but decreased to 234.6±25.4 cpm in AT 1R-AS-ODN treatment group. CONCLUSION:AT 1R-AS-ODN can reverse the increase of c-jun gene expression,proliferation and 3H-Proline incorporation of cardiac fibroblasts induced by AngⅡ.
关 键 词:心肌成纤维细胞 AT1R—AS—ODN 血管紧张素Ⅱ c—jun基因
分 类 号:R542.2[医药卫生—心血管疾病]
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