ANGPTL4对苯肾上腺素诱导的心肌纤维化的调控  

Regulation of phenylephrine-induced cardiac fibrosis by ANGPTL4

作　　者：王立娟[1] 刘晨[2] 许元文[2] WANG Lijuan;LIU Chen;XU Yuanwen(Huiya Hosptial of The First Affiliated Hospital,Sun Yat.Sen University,Huizhou 516000,China)

机构地区：[1]中山大学附属第一医院惠亚医院,广东省惠州市516000 [2]中山大学附属第一医院,广州市510080

出　　处：《实用医学杂志》2017年第12期1939-1942,共4页The Journal of Practical Medicine

摘　　要：目的:探讨ANGPTL4对苯肾上腺素(PE)诱导的心肌纤维化的调控作用。方法:应用PE诱导乳鼠心肌纤维化;通过小干扰RNA转染沉默心肌成纤维细胞ANGPTL4表达,应用Western blot验证沉默效率;CCK8检测心肌成纤维细胞增殖效率;荧光定量PCR检测胶原蛋白Ⅰ(Col1)、结缔组织生长因子(CT-GF)mRNA表达水平改变。结果:PE导致心肌成纤维细胞增殖效率增加,促进Col1及CTGF mRNA表达;ANG-PTL4蛋白沉默进一步促进心肌成纤维细胞增殖及Col1和CTGF mRNA表达。结论:ANGPTL4可抑制PE诱导的心肌纤维化。Objective To study how ANGPTL4modulates phenylephrine(PE)?induced cardiac fibrosis.Methods PE was applied to induce cardiac fibrosis.The knockdown effect of ANGPTL4under PE stimuli wasconfirmed by Western blot;the proliferation of cardiac fibroblast was detected by CCK?8;mRNA levels ofCollagen1(Col1)and connective tissue growth factor(CTGF)were detected by QPCR to investigate the regula?tion of cardiac fibrosis by ANGPTL4.Results PE induced the proliferation of cardiac fibroblast and the up?regula?tion of mRNA levels of Col1and CTGF;ANGPTL4knockdown deteriorated cardiac fibrosis,manifested by the up?regulation of Col1and CTGF.Conclusion ANGPTL4inhibits PE?induced cardiac fibrosis.

关 键 词：心肌纤维化 苯肾上腺素 ANGPTL4 

分 类 号：R542.23[医药卫生—心血管疾病]