• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cellular Physiology and Biochemistry >Epigallocatechin Gallate Attenuated the Activation of Rat Cardiac Fibroblasts Induced by Angiotensin II via Regulating β-Arrestin1
【24h】

Epigallocatechin Gallate Attenuated the Activation of Rat Cardiac Fibroblasts Induced by Angiotensin II via Regulating β-Arrestin1

机译：表没食子儿茶素没食子酸酯通过调节β-Arrestin1减弱血管紧张素II诱导的大鼠心脏成纤维细胞的活化。

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Background/Aims: Angiotensin II (AngII) activated cardiac fibroblasts (CFs) predominantly through AngII subtype 1a receptor (AT1aR). This study was carried out to explore the potential inhibitory effects and mechanisms of epigallocatechin gallate (EGCG) on AngII induced rat CFs. Methods: Viability, proliferation and collagen production of CFs were measured by MTT assay, [3H]-thymidine and [3H]-proline incorporation respectively. β-arrestin1 (βarr1), AT1aR and AT1bR mRNA levels were determined by quantitative PCR. AT1R, Gq, βarr 1/2, phosphorylated kinase C (p-PKC)-delta expressions were detected by western blotting. We blocked βarr1 expression using βarr1 small interfering RNA (siRNA). Results: EGCG inhibited the activation of CFs induced by AngII. βarr1 mRNA level revealed a positive correlation with the viability of CFs. SiRNA targeting βarr1 blocked the activation of CFs. In vitro, AngII increased βarr1 mRNA, total and membrane βarr1 protein expressions, but reduced AT1aR mRNA, global and membrane AT1R, total Gq and cytoplasmic p-PKC-delta levels. Administration of EGCG restored the above abnormalities, whereas Gq levels were not affected. Conclusion: Our findings showed that βarr1 is essential for AngII-mediated activation of CFs. EGCG attenuated CFs activation induced by AngII via regulating βarr1 and thus, modulating AT1aR mediated signaling.
机译：背景/目的：血管紧张素II（AngII）主要通过AngII 1a亚型受体（AT1aR）激活了心脏成纤维细胞（CFs）。本研究旨在探讨表没食子儿茶素没食子酸酯（EGCG）对AngII诱导的大鼠CF的潜在抑制作用及其机制。方法：分别采用MTT法，[ 3 H]-胸苷和[ 3 H]-脯氨酸掺入法测定CFs的活力，增殖和胶原蛋白的产生。通过定量PCR测定β-arrestin1（βarr1），AT1aR和AT1bR mRNA水平。通过蛋白质印迹检测AT1R，Gq，βarr1/2，磷酸化激酶C（p-PKC）-δ表达。我们使用βarr1小干扰RNA（siRNA）阻断了βarr1的表达。结果：EGCG抑制了AngII诱导的CFs活化。 βarr1mRNA水平与CFs的活力呈正相关。靶向βarr1的SiRNA阻止了CF的激活。在体外，AngII增加了βarr1mRNA，总βarr1和膜βarr1蛋白的表达，但降低了AT1aR mRNA，总AT1和膜AT1R，总Gq和细胞质p-PKC-δ水平。 EGCG的施用恢复了上述异常，而Gq水平不受影响。结论：我们的发现表明，βarr1对于AngII介导的CFs激活至关重要。 EGCG通过调节βarr1减弱了AngII诱导的CFs激活，从而调节了AT1aR介导的信号传导。

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