• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Life sciences >Plantainoside D protects adriamycin-induced apoptosis in H9c2 cardiac muscle cells via the inhibition of ROS generation and NF-kB activation
【24h】

Plantainoside D protects adriamycin-induced apoptosis in H9c2 cardiac muscle cells via the inhibition of ROS generation and NF-kB activation

机译：车前草苷D通过抑制ROS生成和NF-kB激活来保护阿霉素诱导的H9c2心肌细胞凋亡

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

Plantainoside D (PD), was isolated from the leaves of Picrorhiza scmphulariiflora (Scrophulariaceae). The anti-oxidative activity of PD was evaluated based on scavenging effects on hydroxyl radicals and superoxide anion radicals. Adriamycin (ADR) is a potent anti-tumor drug known to cause severe cardiotoxicity. Although ADR generates free radicals, the role of free radicals in the development of cardiac toxicity has not been understood. This study was undertaken to investigate the protective effect of PD against ADR-induced apoptosis. In vitro, ADR caused dose-dependent toxicity in H9c2 cardiac muscle cells. Pre-treatment of the cardiac muscle cells with PD significantly reduced ADR-induced apoptosis of cardiac muscle cells. PD inhibited the ROS produced by ADR in the cardiac muscle cells. As well, PD increased GSH(glutathione), compared with ADR. In response to ADR, NF-kB was activated in H9c2 cells. However the treatment of PD reduced the activation of NF-kB. We also observed that the NF-kB inhibitor, PDTC, inhibited the cytotoxic effect on ADR-induced apoptosis in cardiac muscle cells. In parallel, iKBa-dominant negative plasmid-overexpression abrogated ADR-induced apoptosis in H9c2 cardiac muscle cells. In conclusion, these results suggest that Plantaionoside D can inhibit ADR-induced apoptosis in H9C2 cardiac muscle cells via inhibition of ROS generation and NF-kB activation. The pure compound PD can be a potential candidate agent which protects cardiotoxicity in ADR-exposed patients. 500Piantainoside D; adriamycin (ADR); Apoptosis; Reactive oxygen species (ROS); Nuclear factor-kappaB (NF-kB)
机译：车前草苷D（PD）是从Pictorhiza scmphulariiflora（玄参科）的叶子中分离出来的。基于对羟基自由基和超氧阴离子自由基的清除作用，评估PD的抗氧化活性。阿霉素（ADR）是一种有效的抗肿瘤药物，已知会引起严重的心脏毒性。尽管ADR会产生自由基，但自由基在心脏毒性发展中的作用尚不清楚。进行该研究以研究PD对ADR诱导的细胞凋亡的保护作用。在体外，ADR在H9c2心肌细胞中引起剂量依赖性毒性。用PD预处理心肌细胞可显着减少ADR诱导的心肌细胞凋亡。 PD抑制了ADR在心肌细胞中产生的ROS。同样，与ADR相比，PD会增加GSH（谷胱甘肽）。响应ADR，NF-κB在H9c2细胞中被激活。然而，PD的治疗降低了NF-kB的活化。我们还观察到，NF-kB抑制剂PDTC抑制了ADR诱导的心肌细胞凋亡的细胞毒性作用。同时，以iKBa为主的负质粒过表达消除了ADR诱导的H9c2心肌细胞凋亡。总之，这些结果表明，车前子苷D可以通过抑制ROS生成和NF-kB活化来抑制ADR诱导的H9C2心肌细胞凋亡。纯化合物PD可能是保护暴露于ADR的患者心脏毒性的潜在候选药物。 500苦杏仁苷D;阿霉素（ADR）;细胞凋亡;活性氧（ROS）;核因子-κB（NF-kB）

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