...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>FEBS Open Bio >Panax notoginseng saponins ameliorate cisplatin‐induced mitochondrial injury via the HIF‐1α/mitochondria/ROS pathway
【24h】

Panax notoginseng saponins ameliorate cisplatin‐induced mitochondrial injury via the HIF‐1α/mitochondria/ROS pathway

机译：Panax Notinseng Saponins通过HIF-1α/ Mitochondria / ROS路径改善了顺铂诱导的线粒体损伤

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

摘要

Cisplatin is a major antineoplastic drug that is used to treat solid tumors, but its use is restricted by its nephrotoxicity. Such cisplatin‐induced nephrotoxicity (CIN) is believed to occur primarily through mitochondrial damage and reactive oxygen species (ROS) generation. Our previous studies have indicated that Panax notoginseng saponins (PNSs) mitigate CIN by enhancing hypoxia‐inducible factor 1α (HIF‐1α)‐induced mitochondrial autophagy. In this study, the role of the HIF‐1α/mitochondria/ROS pathway in PNSs protection against CIN was investigated using a rat model. A CIN model was generated by giving rats intraperitoneal injections with cisplatin (a single dose) and then treating them with or without 2‐methoxyestradiol (HIF‐1α inhibitor) and PNSs. We then measured ROS levels, superoxide dismutase, glutathione, catalase malondialdehyde and nitric oxide (to evaluate oxidative stress) and ATP, mitochondrial membrane potential and mitochondrial permeability transition pore opening (to evaluate mitochondrial function) in kidneys at different time points. We observed that PNSs remarkably reduced the levels of ROS, malondialdehyde and nitric oxide, as well as the opening of mitochondrial permeability transition pore, which is increased by cisplatin and further increased by HIF‐1α inhibition. In addition, PNSs increased the levels of superoxide dismutase, catalase and glutathione, as well as ATP and mitochondrial membrane potential in renal tissues; these are all reduced by cisplatin and further reduced by HIF‐1α inhibition. In conclusion, we demonstrate here that PNSs protects against mitochondrial damage induced by cisplatin through HIF‐1α/mitochondria/ROS.
机译：顺铂是一种主要的抗肿瘤药物，用于治疗实体瘤，但其使用受其肾毒性的限制。认为这种顺铂诱导的肾毒性（CIN）主要通过线粒体损伤和反应性氧（ROS）产生。我们以前的研究表明，通过增强缺氧诱导因子1α（HIF-1α）诱导的线粒体自噬，Panax Notinseng Saponins（PNSS）减轻了Cin。在本研究中，使用大鼠模型研究了HIF-1α/线粒体/ ROS途径在PNSS保护对CIN的作用。通过用顺铂（单剂量）腹腔注射大鼠，然后用或没有2-甲氧基雌二醇（HIF-1α抑制剂）和PNSS来生成CIN模型。然后测量ROS水平，超氧化物歧化酶，谷胱甘肽，过氧化氢酶丙二醛和一氧化氮（以评估氧化应激）和ATP，线粒体膜电位和线粒体渗透性转变孔口（以评估不同时间点的肾脏中的线粒体功能）。我们观察到PNSS显着降低了ROS，丙二醛和一氧化氮的水平，以及线粒体渗透性过渡孔的开口，其由顺铂增加，并通过HIF-1α抑制进一步增加。此外，PNSS增加了超氧化物歧化酶，过氧化氢酶和谷胱甘肽的水平，以及肾组织中的ATP和线粒体膜电位;这些都是通过顺铂的减少，并通过HIF-1α抑制进一步减少。总之，我们在此证明PNSS通过HIF-1α/ Mitochondria / ROS免受顺铂诱导的线粒体损伤。

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