基础医学与临床 ›› 2009, Vol. 29 ›› Issue (12): 1310-1313.

• 研究论文 • 上一篇    下一篇

阿司匹林抑制内皮素-1诱导的大鼠心脏成纤维细胞增殖

张志国 杨力 郑亚萍 赵艳峰   

  1. 漯河医学高等专科学校
  • 收稿日期:2008-11-26 修回日期:2009-04-21 出版日期:2009-12-20 发布日期:2009-12-20
  • 通讯作者: 张志国

ASPIRIN INHIBITE THE PROLIFERATION OF RAT CARDIAC FIBROBLASTS INDUCED BY ENDOTHELIN-1

Zhi-guo ZHANG, Li YANG, Ya-ping ZHENG, Yan-feng ZHAO   

  1. Luohe Medical College
  • Received:2008-11-26 Revised:2009-04-21 Online:2009-12-20 Published:2009-12-20
  • Contact: Zhi-guo ZHANG,

摘要: 目的 探讨阿司匹林(Aspirin)对内皮素-1(ET-1)诱导的大鼠心脏成纤维细胞(CFs)增殖的干预作用及可能机制。方法 经差速贴壁法培养的新生大鼠CFs,随机分为7组:对照组、ET-1组、阿司匹林组、ET-1+ 阿司匹林1、2、5和10 mmol·L-1组。用四氮唑盐(MTT)法测定CFs数目,流式细胞仪检测CFs细胞周期,液体闪烁计数仪测定CFs 3H-脯氨酸掺入率,硝酸还原酶法测定细胞培养上清液中NO含量。结果 与对照组相比,10-7 mol·L-1 ET-1能显著促CFs增值及[3H]-Proline掺入率,降低CFs生成NO2-/NO3-的量(均P < 0.01),1~10 mmol·L-1 阿司匹林呈浓度依赖性的缓解上述变化(均P < 0.05); ET-1能显著提高S期细胞百分率(P < 0.01),10 mmol·L-1 阿司匹林抑制ET-1诱导S期细胞百分率上升(P < 0.01)。结论 阿司匹林抑制ET-1诱导的CFs增殖及胶原合成可能和NO生成有关。

Abstract: Aim: To investigate the effect of Aspirin on endothelin-1 induced proliferation of cardiac fibroblasts (CFs). Methods: Isolated and cultured CFs from neonatal Sprague-Dawley rats (SD) were randomly divided into 7 groups: ①control, ②ET-1, ③Aspirin, ④ET-1+ Aspirin 1mmol/L, ⑤ET-1+ Aspirin 2mmol/L, ⑥ET-1+ Aspirin 5mmol/L and ⑦ET-1+ Aspirin1 10mmol/L. CFs were counted by MTT assay. Cell cycle distribution was determined with a flow cytometer (FCM). [3H]-Proline incorporation was evaluated by scintillation counting. Nitric oxide (NO) was measured by colorimetry. Results: 10-7mol/L ET-1 significantly increased the number of CFs and [3H]-Pro incorporation and decreased NO2-/NO3- secretion compared with the control group (P < 0.01). 1-10mmol/L Aspirin inhibited the effects of ET-1 on CFs in a concentration-dependent manner (P < 0.05 vs ET-1). In the ET-1 group, the percentage of cells in the S phase was higher than control, which was inhibited by 10mmol/L Aspirin (P< 0.01 vs ET-1 and control). Conclusion: Aspirin can restrain the proliferation and collagen synthesis of cardiac fibroblasts induced by endothelin-1, and this effect may be partially mediated by NO.