...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The Journal of toxicological sciences >Melatonin antagonizes oxidative stress-induced mitochondrial dysfunction in retinal pigmented epithelium cells via melatonin receptor 1 (MT1)
【24h】

Melatonin antagonizes oxidative stress-induced mitochondrial dysfunction in retinal pigmented epithelium cells via melatonin receptor 1 (MT1)

机译：褪黑素通过褪黑素受体1（MT1）拮抗视网膜着色上皮细胞中的氧化应激诱导的线粒体功能障碍

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

High energy-consumption in retinal pigmented epithelium (RPE) cells poses oxidative stress (OS) and contributes to mitochondrial dysfunction (MD) for retinal degeneration-associated diseases. In the present study, we evaluated the protective role of Melatonin, a natural antioxidant, against the hydrogen peroxide WOO-induced damage to RPE cells. The cellular viability, apoptosis, the expression of apoptosis-associated proteins and mitochondrial function were examined in the retinal ARPE-19 cells, post the treatment with H2O2 or (and) with Melatonin. The regulation by Melatonin receptor 1 (MTI) on the Melatonin-mediated protection was also examined via MT1 knockdown with siRNA. Results demonstrated that Melatonin significantly ameliorated cell viability reduction, reduced apoptosis and downregulated the apoptosis-associated proteins in H2O2 -treated ARPE-19 cells. The H2O2-induced mitochondrial dysfunction was also significantly blocked by the Melatonin treatment, presenting as a reduced accumulation of reactive oxygen species (ROS) and mitochondrial superoxide and an ameliorated reduction of mitochondrial membrane potential (MMP). In addition, the knockdown of MT1 with MT1-specific siRNA inhibited the Melatonin-mediated protection against OS damage in ARPE-19 cells. In summary, we confirmed the protective role of Melatonin against H2O2-induced mitochondrial dysfunction in RPE cells. MT1 knockdown blocked such protective role of Melatonin. It is implied that Melatonin exerts a protective role against oxidative stress via Melatonin-MT1 signaling in RPE cells.
机译：视网膜着色上皮（RPE）细胞的高能量消耗造成氧化应激（OS），有助于视网膜变性相关疾病的线粒体功能障碍（MD）。在本研究中，我们评估了褪黑激素，天然抗氧化剂，抗过氧化氢源对RPE细胞损伤的保护作用。在视网膜ARPE-19细胞中检查了细胞活力，细胞凋亡，凋亡相关蛋白和线粒体功能的表达，用H2O2或（和）用褪黑素处理。通过使用SiRNA的MT1敲低检查褪黑激素受体1（MTI）对褪黑激素介导的保护的调节。结果表明，褪黑激素显着​​改善了细胞可活力，降低细胞凋亡，并下调了H 2 O 2 -Treated ARPE-19细胞中的凋亡相关蛋白。通过褪黑素处理，H2O2诱导的线粒体功能障碍也显着阻断，呈递作为反应性氧物质（ROS）和线粒体超氧化物的减少的积累和线粒体膜电位（MMP）的改善降低。此外，使用MT1特异性siRNA的MT1敲低抑制了褪黑激素介导的抗孢子蛋白介导的ARPE-19细胞损伤的保护。总之，我们确认褪黑素对RPE细胞中H2O2诱导的线粒体功能障碍的保护作用。 MT1敲低阻断了褪黑素的这种保护作用。暗示褪黑激素在RPE细胞中通过褪黑激素-MT1信号传导对抗氧化应激的保护作用。

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