考尼伐坦抑制精氨酸血管加压素诱导的心脏成纤维细胞增殖及胶原表达  

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

作　　者：谢永进[1] 孙志军[1] 盖鲁粤[1] 

机构地区：[1]解放军总医院心血管内科,北京100853

出　　处：《细胞与分子免疫学杂志》2013年第5期477-480,共4页Chinese Journal of Cellular and Molecular Immunology

摘　　要：目的探讨大鼠心脏成纤维细胞(CFs)经精氨酸血管加压素(AVP)及其受体拮抗剂考尼伐坦(CON)干预后,细胞的增殖和细胞中Ⅰ、Ⅲ型胶原蛋白表达的变化。方法采用胶原酶Ⅱ消化法、差速贴壁法、差速脱壁法获取并纯化CFs,应用CCK-8活细胞计数试剂盒检测细胞活性,RT-PCR方法检测细胞中Ⅰ型胶原蛋白α1链(COL1A1)和Ⅲ型胶原蛋白α1链(COL3A1)mRNA的变化,Western blot法检测COL1A1、COL3A1蛋白表达的变化。结果干预培养的CFs 24h后,10-7mol/LAVP可显著促进CFs细胞增殖(P<0.01),而10-7mol/L CON可显著抑制这一作用(P<0.01)。干预培养的CFs 12h后,10-7mol/L AVP可诱导CFs COL1A1、COL3A1mRNA表达显著增加,同时蛋白表达亦显著增加,而10-7mol/L的CON可抑制这些作用。结论 AVP可促进CFs的细胞增殖和COL1A1、COL3A1mRNA和蛋白表达,而CON可部分抑制这种作用。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 II1. 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 COI_3A1 mRNA were detected by RT-PCR, and the protein levels of （collagen type 1, alpha 1, COL1A1 ） and COL3A1 were as- sessed by Western blotting. Results At 24 h after intervention, 10-7 mol/L AVP promoted the proliferation of CFs in compari- son 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 inter- vention, 10-7 mol/L AVP significantly enhanced the expressions of COL1A1 and COI.3A1 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 COL3A] expressions at both mRNA and protein levels, while CON could restrain the AVP effects partially.

关 键 词：精氨酸血管加压素 考尼伐坦 胶原 心脏成纤维细胞 

分 类 号：R392.11[医药卫生—免疫学] Q251[医药卫生—基础医学]