• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cellular Physiology and Biochemistry >Stimulation of Eryptosis, the Suicidal Erythrocyte Death, by Costunolide
【24h】

Stimulation of Eryptosis, the Suicidal Erythrocyte Death, by Costunolide

机译：Costunolide刺激隐匿性自杀性红细胞死亡

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

摘要

Background/Aims The sesquiterpene lactone Costunolide is effective against various disorders including inflammation and malignancy. The substance is effective in part by triggering suicidal death or apoptosis of tumor cells. Mechanisms involved include altered function of transcription factors and mitochondria. Erythrocytes lack nuclei and mitochondria but are – in analogy to apoptosis of nucleated cells – able to enter suicidal erythrocyte death or eryptosis, characterized by cell shrinkage and cell membrane scrambling with phosphatidylserine translocation to the erythrocyte surface. Triggers of eryptosis include increase of cytosolic Ca2+ activity ([Ca2+]i), oxidative stress and ceramide. The present study explored, whether Costunolide induces eryptosis and, if so, to shed light on the mechanisms involved. Methods Phosphatidylserine exposure at the cell surface was estimated from annexin-V-binding, cell volume from forward scatter, [Ca2+]i from Fluo3-fluorescence, reactive oxygen species (ROS) formation from 2’,7’-dichlorodihydrofluorescein (DCF)-dependent fluorescence, and ceramide abundance utilizing specific antibodies. Results A 48 hours exposure of human erythrocytes to Costunolide (15 µg/ml) significantly enhanced the percentage of annexin-V-binding cells, significantly decreased forward scatter and significantly increased Fluo3-fluorescence, DCF-fluorescence, and ceramide abundance. The effect of Costunolide on annexin-V-binding was significantly blunted by removal of extracellular Ca2+. Conclusion Costunolide triggers cell shrinkage and phospholipid scrambling of the erythrocyte cell membrane, an effect at least in part due to Ca2+ entry and paralleled by oxidative stress and ceramide formation.
机译：背景/目的倍半萜内酯Costunolide对多种疾病有效，包括炎症和恶性肿瘤。该物质通过触发自杀性死亡或肿瘤细胞凋亡而部分有效。涉及的机制包括转录因子和线粒体功能的改变。红细胞缺乏细胞核和线粒体，但（类似于有核细胞的凋亡）能够进入自杀性红细胞死亡或隐匿，其特征是细胞萎缩和细胞膜争夺，磷脂酰丝氨酸易位至红细胞表面。加密的触发因素包括胞质Ca2 +活性（[Ca2 +] i），氧化应激和神经酰胺的增加。本研究探讨了Costunolide是否会诱导加密作用，如果是的话，则可以阐明所涉及的机制。方法根据膜联蛋白-V-结合，前向散射的细胞体积，Fluo3-荧光的[Ca2 +] i，2'，7'-二氯二氢荧光素（DCF）-形成的活性氧（ROS）估算细胞表面的磷脂酰丝氨酸暴露量。依赖的荧光和利用特定抗体的神经酰胺丰度。结果人类红细胞暴露于Costunolide（15 µg / ml）48小时会显着增加膜联蛋白V结合细胞的百分比，显着降低前向散射并显着增加Fluo3荧光，DCF荧光和神经酰胺丰度。通过去除细胞外Ca2 +，Costunolide对膜联蛋白-V结合的作用明显减弱。结论Costunolide触发红细胞膜的细胞收缩和磷脂加扰，这种作用至少部分是由于Ca2 +进入并与氧化应激和神经酰胺形成平行。

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