...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The journals of gerontology.Series A. Biological sciences and medical sciences >The Redox-sensitive Induction of the Local Angiotensin System Promotes Both Premature and Replicative Endothelial Senescence: Preventive Effect of a Standardized Crataegus Extract
【24h】

The Redox-sensitive Induction of the Local Angiotensin System Promotes Both Premature and Replicative Endothelial Senescence: Preventive Effect of a Standardized Crataegus Extract

机译：局部血管紧张素系统的氧化还原敏感诱导促进早熟和复制性内皮衰老：标准化山楂提取物的预防作用。

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

Endothelial senescence, characterized by an irreversible cell cycle arrest, oxidative stress, and downregulation of endothelial nitric oxide synthase (eNOS), has been shown to promote endothelial dysfunction leading to the development of age-related vascular disorders. This study has assessed the possibility that the local angiotensin system promotes endothelial senescence in coronary artery endothelial cells and also the protective effect of the Crataegus extract WS1442, a quantified hawthorn extract. Serial passaging from P1 to P4 (replicative senescence) and treatment of P1 endothelial cells with the eNOS inhibitor L-NAME (premature senescence) promoted acquisition of markers of senescence, enhanced ROS formation, decreased eNOS expression, and upregulation of angiotensin-converting enzyme (ACE) and AT1 receptors. Increased SA-beta-gal activity and the upregulation of ACE and AT1R in senescent cells were prevented by antioxidants, an ACE inhibitor, and by an AT1 receptor blocker. WS1442 prevented SA-beta-gal activity, the downregulation of eNOS, and oxidative stress in P3 cells. These findings indicate that the impairment of eNOS-derived nitric oxide formation favors a pro-oxidant response triggering the local angiotensin system, which, in turn, promotes endothelial senescence. Such a sequence of events can be effectively inhibited by a standardized polyphenol-rich extract mainly by targeting the oxidative stress.
机译：内皮细胞衰老的特征是不可逆的细胞周期停滞，氧化应激和内皮一氧化氮合酶（eNOS）的下调，可促进内皮功能障碍，导致与年龄相关的血管疾病的发展。这项研究评估了局部血管紧张素系统促进冠状动脉内皮细胞的内皮衰老的可能性，并评估了山楂提取物WS1442（一种定量的山楂提取物）的保护作用。从P1到P4的连续传代（复制性衰老）和用eNOS抑制剂L-NAME处理P1内皮细胞（过早衰老）促进了衰老标记的获得，ROS形成增强，eNOS表达降低以及血管紧张素转化酶的上调（ ACE）和AT1受体。抗氧化剂，ACEI抑制剂和AT1受体阻滞剂可防止衰老细胞中SA-beta-gal活性的增加以及ACE和AT1R的上调。 WS1442阻止了SA-beta-gal活性，eNOS的下调和P3细胞中的氧化应激。这些发现表明，eNOS衍生的一氧化氮形成的损伤促进了促氧化剂反应，从而触发了局部血管紧张素系统，进而促进了内皮的衰老。主要通过针对氧化应激，可以通过标准化的富含多酚的提取物有效地抑制这种事件序列。

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