...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Die Pharmazie >Nifedipine inhibits angiotensin II-induced cardiac fibrosis via downregulating Nox4-derived ROS generation and suppressing ERK1/2, JNK signaling pathways
【24h】

Nifedipine inhibits angiotensin II-induced cardiac fibrosis via downregulating Nox4-derived ROS generation and suppressing ERK1/2, JNK signaling pathways

机译：硝苯地平通过下调Nox4衍生的ROS生成并抑制ERK1 / 2，JNK信号通路来抑制血管紧张素II诱导的心脏纤维化

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Nifedipine, a classic L-type dihydropyridine calcium channel blocker (CCB), has been reported to possess multiple cardioprotective properties. However, little is known about the effects of nifedipine on cardiac fibrosis induced by angiotensinII (AngII) and the detailed molecular mechanisms. In this study, we found that nifedipine attenuated AngII-induced cardiac fibrosis in vitro via inhibiting the proliferation, differentiation of cardiac fibroblasts and antagonizing the upregulation of extracellular matrix (ECM) protein fibronectin (FN) and the pro-fibrotic cytokine connective tissue growth factor (CTGF). Furthermore, nifedipine suppressed the upregulation of NAD(P)H oxidase 4 (Nox4) and the production of reactive oxygen species (ROS) induced by AngII. In addition, it markedly inhibited the phosphorylation of extracellular signal-regulate kinases 1/2 (ERK1/2) and c-Jun NH(2)-terminal kinase (JNK) stimulated by AngII. However, nifedipine exhibited no effect on the variation of intracellular Ca2+ concentration ([Ca2+]i). These results suggested that (1) nifedipine inhibited cardiac fibrosis induced by AngII; (2) the anti-fibrotic effects of nifedipine may be mediated by interfering with the production of ROS and the activation of ERK1/2 and JNK signaling pathways; (3) the classic calcium channel blocking action of nifedipine may not be involved in the anti-fibrotic activities.
机译：硝苯地平是一种经典的L型二氢吡啶钙通道阻滞剂（CCB），据报道具有多种心脏保护特性。然而，关于硝苯地平对血管紧张素II（AngII）诱导的心脏纤维化的作用及其详细的分子机制知之甚少。在这项研究中，我们发现硝苯地平通过抑制心脏成纤维细胞的增殖，分化并拮抗细胞外基质（ECM）蛋白纤连蛋白（FN）和促纤维化细胞因子结缔组织生长因子的表达而在体外减轻了AngII诱导的心脏纤维化。 （CTGF）。此外，硝苯地平抑制了AngII诱导的NAD（P）H氧化酶4（Nox4）的上调和活性氧（ROS）的产生。此外，它显着抑制AngII刺激的细胞外信号调节激酶1/2（ERK1 / 2）和c-Jun NH（2）-末端激酶（JNK）的磷酸化。但是，硝苯地平对细胞内Ca2 +浓度（[Ca2 +] i）的变化没有影响。这些结果表明（1）硝苯地平抑制AngII诱导的心脏纤维化; （2）硝苯地平的抗纤维化作用可能是通过干扰ROS的产生以及ERK1 / 2和JNK信号通路的激活来介导的; （3）硝苯地平经典的钙通道阻滞作用可能不参与抗纤维化活性。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号