...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Shock: Molecular, cellular, and systemic pathobiological aspects and therapeutic approaches = The official journal of the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies >Glutathione depletion-induced neutrophil apoptosis is caspase 3 dependent.
【24h】

Glutathione depletion-induced neutrophil apoptosis is caspase 3 dependent.

机译：谷胱甘肽depletion-induced中性粒细胞凋亡半胱天冬酶3相关的。

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

Resolving inflammation is a vital step in preventing the persistence of inflammatory disorders. Neutrophils play a major role in tissue damage associated with an inflammatory response. Their death by apoptosis is central to the final resolution of this response. Thiol depletion with diethylmaleate (DEM) or diamide represent important triggers for neutrophil apoptosis. The mechanism by which this process occurs remains unknown. The apoptotic cascade is associated with a number of cellular changes, including caspase activation and mitochondrial permeability. The aims of this study were to determine the role of mitochondrial permeability and the caspase cascade in thiol depletion-induced neutrophil apoptosis. Total cellular glutathione was reduced by DEM and diamide. This reduction was associated with neutrophil apoptosis and an increase in caspase 3 activity. The effects of DEM were blocked by the caspase 3 inhibitor, Z-DEVD-FMK. Mitochondrial permeability that occurred was also increased during this induction of apoptosis. Bongkrekic acid, a mitochondrial membrane stabilizer, inhibited DEM-induced apoptosis. The inhibitors' effects of LPS or GM-CSF on spontaneous neutrophil apoptosis was reversed by DEM, which was mediated by an increase in caspase 3 activity and independent of mitochondrial disruption. Caspase activation is an important step in glutathione depletion-induced apoptosis in resting and inflammatory neutrophils. Regulation of caspase activity may represent a possible target to trigger apoptosis and resolve inflammatory disorders.
机译：解决炎症是至关重要的一步预防炎症的持久性障碍。组织损伤与炎症有关响应。这种反应的最终解决。与diethylmaleate损耗(民主党)或二酰胺代表中性粒细胞的重要诱因细胞凋亡。发生仍然未知。相关的细胞数量的变化,包括细胞凋亡蛋白酶活化和线粒体渗透率。确定线粒体通透性的作用硫醇和半胱天冬酶级联depletion-induced中性粒细胞凋亡。细胞谷胱甘肽降低了民主党二酰胺。中性粒细胞凋亡以及细胞凋亡蛋白酶3活动。半胱天冬酶3抑制剂,Z-DEVD-FMK。渗透率发生也增加在诱导细胞凋亡。酸、线粒体膜稳定剂,抑制DEM-induced细胞凋亡。有限合伙人或gm - csf对自然的影响中性粒细胞凋亡被民主党逆转,是由增加半胱天冬酶3活动和独立的线粒体紊乱。半胱天冬酶激活是一个重要的一步谷胱甘肽depletion-induced细胞凋亡在休息和炎症性中性粒细胞。半胱天冬酶的活动可能代表一个可能的目标引发细胞凋亡和解决炎症性疾病。

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