文章摘要
谷颖,金鑫,李霞,沈彩云,石朋.HO-1对AngⅡ诱导大鼠心肌纤维化的影响[J].济宁医学院学报,2019,42(6):395-398
HO-1对AngⅡ诱导大鼠心肌纤维化的影响
Effect of HO-1 on AngⅡ-induced myocardial fibrosis in rats
投稿时间:2019-05-30  
DOI:10.3969/j.issn.1000-9760.2019.06.004
中文关键词: 血红素氧合酶-1;心肌纤维化;心肌成纤维细胞;血管紧张素Ⅱ
英文关键词: Heme oxygenase-1;Myocardial fibrosis;Cardiac fibroblasts;AngiotensinⅡ
基金项目:
作者单位E-mail
谷颖 济宁医学院附属医院, 济宁 272029  
金鑫 济宁医学院附属医院, 济宁 272029  
李霞 济宁医学院附属医院, 济宁 272029  
沈彩云 济宁医学院附属医院, 济宁 272029  
石朋 济宁医学院附属医院, 济宁 272029 bler-8456@163.com 
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中文摘要:
      目的 探讨血红素氧合酶-1(HO-1)对血管紧张素Ⅱ(AngⅡ)诱导大鼠心肌纤维化的作用。方法 培养Wistar大鼠心肌成纤维细胞(cardiac fibroblasts,CFs),随机分为4组:正常对照组、AngⅡ组(加入AngⅡ)、Hemin组(加入AngⅡ和HO-1诱导剂氯化血红素hemin)和ZnppIX组(加入AngⅡ和HO-1抑制剂锌原卟啉-9 ZnppIX),四甲基偶氮唑盐比色法(MTT)检测各组细胞的增殖率,Western blot检测各组细胞HO-1蛋白的表达。结果 AngⅡ组较正常对照组心肌成纤维细胞增殖率显著升高(P<0.01);与AngⅡ组比较,Hemin组细胞增殖率显著下降(P<0.01),HO-1蛋白表达水平显著升高(P<0.01);与AngⅡ组比较,ZnppIX组细胞增殖率无明显变化(P>0.05),HO-1蛋白表达水平降低(P<0.01)。结论 HO-1对AngⅡ诱导的大鼠心肌纤维化具有抑制作用。
英文摘要:
      Objective To investigate the effect of heme oxygenase-1 (HO-1) on angiotensin Ⅱ (AngⅡ) -induced myocardial fibrosis in rats.Methods Cultured neonatal Wistar rats' cardiac fibroblasts (CFs) were randomly divided into 4 groups,the normal group,the AngⅡ group (added AngⅡ),the Hemin group (added AngⅡ and hemin which could induce more HO-1) and the ZnppIX group (added AngⅡ and Zinc protoporphyrin-9 which could reduce HO-1).The proliferation of cardiac fibroblasts of each group was detected by MTT assay.The expression of HO-1 protein in cardiac fibroblasts was detected by Western blot.Results The proliferation rate of cardiac fibroblasts in AngⅡ group was significantly higher than that in normal group (P<0.01).The proliferation rate of Hemin group was significantly lower than that of AngⅡ group (P<0.01),while the expression of HO-1 protein was significantly increased (P<0.01).However,there was no significant change in cell proliferation rate in the ZnppIX group compared with the AngⅡ group (P>0.01),while the expression of HO-1 protein was significantly decreased (P<0.01).Conclusion HO-1 could inhibit the AngⅡ-induced myocardial fibrosis in rats.
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