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

Investigation of angiotensin Ⅱ typeⅠ receptor antisense oligonucleotide on reversing proliferation and collagen synthesis of cardiac fibroblasts

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.