[考尼伐坦抑制精氨酸加压素诱导的心脏成纤维细胞的细胞增殖和胶原蛋白生成]

[Conivaptan inhibites cell proliferation and collagen production of cardiac fibroblasts induced by arginine vasopressin].

作者信息

Xie Yongjin, Sun Zhijun, Gai Luyue

机构信息

Department of Cardiology, General Hospital of PLA, Beijing 100853, China.

出版信息

Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2013 May;29(5):477-80.

PMID:23643265

Abstract

OBJECTIVE

To investigate the effects of arginine vasopressin (AVP) and its receptor antagonist conivaptan (CON) on the proliferation of cardiac fibroblasts (CFs) and the production of collagen I and III.

METHODS

CFs were isolated by collagenase II method and purified with differential attachment and detachment methods. The cell viability of CFs after AVP and/or CON administration was assessed by cell counting kit-8 (CCK-8). The expressions of COL1A1 and COL3A1 mRNA were detected by RT-PCR, and the protein levels of (collagen type 1, alpha 1, COL1A1) and COL3A1 were assessed by Western blotting.

RESULTS

At 24 h after intervention, 10(-7); mol/L AVP promoted the proliferation of CFs in comparison with that in control group (P<0.01), and 10(-7); mol/L CON inhibited the effect significantly (P<0.01). At 12 h after intervention, 10(-7); mol/L AVP significantly enhanced the expressions of COL1A1 and COL3A1 at both mRNA and protein levels, and 10(-7); mol/L CON inhibited the effect again.

CONCLUSION

AVP promoted the proliferation of CFs and enhanced the COL1A1 and COL3A1 expressions at both mRNA and protein levels, while CON could restrain the AVP effects partially.

摘要

目的

探讨精氨酸加压素（AVP）及其受体拮抗剂考尼伐坦（CON）对心脏成纤维细胞（CFs）增殖及Ⅰ型和Ⅲ型胶原蛋白产生的影响。

方法

采用Ⅱ型胶原酶法分离CFs，并用差速贴壁和去贴壁法进行纯化。通过细胞计数试剂盒-8（CCK-8）评估给予AVP和/或CON后CFs的细胞活力。采用逆转录-聚合酶链反应（RT-PCR）检测COL1A1和COL3A1 mRNA的表达，并用蛋白质印迹法评估Ⅰ型胶原蛋白α1（COL1A1）和COL3A1的蛋白水平。

结果

干预24小时后，10⁻⁷ mol/L AVP与对照组相比促进了CFs的增殖（P<0.01），而10⁻⁷ mol/L CON显著抑制了该作用（P<0.01）。干预12小时后，10⁻⁷ mol/L AVP在mRNA和蛋白水平均显著增强了COL1A1和COL3A1的表达，10⁻⁷ mol/L CON再次抑制了该作用。