• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Life sciences >Involvement of hydrogen peroxide in mistletoe lectin-II-induced apoptosis of myeloleukemic U937 cells.
【24h】

Involvement of hydrogen peroxide in mistletoe lectin-II-induced apoptosis of myeloleukemic U937 cells.

机译：过氧化氢参与槲寄生凝集素II诱导的髓性U937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

Mistletoe lectin-II, a major component of Korean mistletoe (Viscum album var. coloratum) induces apoptotic death in cancer cells. In this study, we demonstrated that lectin-II induced the generation of pro-oxidants and thus resulted in the apoptotic death of human myeloleukemic U937 cells. We observed that lectin-II-induced apoptotic death was inhibited by antioxidants including reduced glutathione (GSH), N-acetylcysteine (NAC), ebselen, mnTBP, catalase and pyrrolidine dithiocarbamate (PDTC). GSH and NAC also abolished the apoptotic DNA ladder pattern fragmentation of U937 cells after lectin-II stimulation. Obviously, lectin-II treatment of cells resulted in a remarkable generation of intracellular hydrogen peroxide (H2O2) as an early event, which was monitored fluorimetrically using scopoletin-horse radish peroxidase (HRP) assay and peroxide-sensitive fluorescent probe, DCF-DA. In addition, antioxidants inhibited the activation of c-Jun N-terminal kinase (JNK)/stress-activated protein kinase (SAPK) aswell as cytosolic release of cytochrome c by mistletoe lectin-II. Moreover, lectin-II-induced activation of caspase-9 and 3-like protease and cleavage of poly(ADP-ribose) polymerase (PARP) were inhibited by pretreatment of cells with thiol antioxidants, GSH and NAC. Taken together, these results suggest that Korean mistletoe lectin-II is a strong inducer of pro-oxidant generation such as H2O2, which mediates the JNK/SAPK activation, cytochrome c release, activation of caspase-9 and caspase 3-like protease, and PARP cleavage in human myeloleukemic U937 cells.
机译：槲寄生凝集素II是韩国槲寄生（Viscum album var。coloratum）的主要成分，可诱导癌细胞凋亡。在这项研究中，我们证明了凝集素II诱导了促氧化剂的产生，并因此导致了人类骨髓白血病U937细胞的凋亡性死亡。我们观察到，凝集素II诱导的凋亡死亡被抗氧化剂抑制，包括减少的谷胱甘肽（GSH），N-乙酰半胱氨酸（NAC），依布硒啉，mnTBP，过氧化氢酶和吡咯烷二硫代氨基甲酸酯（PDTC）。 GSH和NAC还消除了凝集素II刺激后U937细胞的凋亡DNA梯形图片段化。显然，凝集素II处理细胞会导致细胞内过氧化氢（H2O2）的大量产生，这是早期事件，可使用碱-马萝卜过氧化物酶（HRP）测定法和过氧化物敏感性荧光探针DCF-DA对其进行荧光监测。此外，抗氧化剂可以抑制槲寄生凝集素II激活c-Jun N末端激酶（JNK）/应激激活蛋白激酶（SAPK）以及细胞色素c的胞质释放。此外，通过用硫醇抗氧化剂，GSH和NAC预处理细胞，可抑制凝集素II诱导的caspase-9和3-like蛋白酶的活化以及聚（ADP-核糖）聚合酶（PARP）的裂解。综上所述，这些结果表明韩国槲寄生凝集素-II是促氧化剂生成的强诱导剂，例如H2O2，它介导JNK / SAPK激活，细胞色素c释放，caspase-9和caspase 3样蛋白酶的激活，以及人骨髓白血病U937细胞中的PARP裂解。

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