首页> 外文期刊>Cellular Physiology and Biochemistry >Sulindac Sulfide – Induced Stimulation of Eryptosis
【24h】

Sulindac Sulfide – Induced Stimulation of Eryptosis

机译:舒林酸硫化物-诱导的隐匿性刺激

获取原文
           

摘要

biBackground/i/b Sulindac sulfide, a non-steroidal anti-inflammatory drug (NSAID), stimulates apoptosis of tumor cells and is thus effective against malignancy. In analogy to apoptosis of nucleated cells, erythrocytes may undergo eryptosis, an apoptosis-like suicidal erythrocyte death, characterized by cell shrinkage and cell membrane scrambling with phosphatidylserine-exposure at the cell surface. Stimulators of eryptosis include increase of cytosolic Casup2+/sup-activity ([Casup2+/sup]subi/sub) and ceramide formation. The present study explored, whether sulindac sulfide stimulates eryptosis. biMethods/i/b [Casup2+/sup]subi/sub was estimated from Fluo-3 fluorescence, cell volume from forward scatter, phosphatidylserine-exposure from binding of fluorescent annexin-V, hemolysis from hemoglobin release, and ceramide abundance utilizing fluorescent antibodies. biResults/i/b A 48 h exposure to sulindac sulfide (≤ 20 µM) was followed by significant increase of [Casup2+/sup]subi/sub, enhanced ceramide abundance, decreased forward scatter and increased percentage of annexin-V-binding erythrocytes. Sulindac sulfide triggered slight but significant hemolysis. Removal of extracellular Casup2+/sup significantly blunted, but did not abrogate the effect of sulindac sulfide (20 µM) on annexin-V-binding. biConclusion/i/b Sulindac sulfide stimulates the suicidal death of erythrocytes or eryptosis, an effect paralleled by Casup2+/sup-entry, ceramide formation, cell shrinkage and phosphatidylserine-exposure.
机译:背景 舒林酸硫化物是一种非甾体类抗炎药(NSAID),可刺激肿瘤细胞凋亡,因此对恶性肿瘤有效。与有核细胞的凋亡类似,红细胞可能会发生隐匿性凋亡,这是一种类似凋亡的自杀性红细胞死亡,其特征是细胞收缩和细胞膜在磷脂酰丝氨酸暴露于细胞表面的过程中变得混乱。加密的刺激物包括增加胞质Ca 2 + -活性([Ca 2 + ] i )和神经酰胺的形成。本研究探讨了舒林酸硫化物是否刺激隐匿性。 方法 [Ca 2 + ] i 由Fluo-3荧光,向前散射的细胞量,磷脂酰丝氨酸估计-暴露于荧光膜联蛋白-V的结合,血红蛋白释放引起的溶血和利用荧光抗体的神经酰胺丰度。 结果 暴露于舒林酸硫化物(≤20 µM)48小时后,[Ca 2 + ] i < / sub,增强了神经酰胺的丰度,减少了前向散射并增加了膜联蛋白-V-结合红细胞的百分比。舒林酸硫化物引起轻微但明显的溶血。细胞外Ca 2 + 的去除明显变钝,但没有消除舒林酸硫化物(20 µM)对膜联蛋白-V-结合的影响。 结论 舒林酸硫化物刺激红细胞自杀死亡或隐匿性,与Ca 2 + 进入,神经酰胺形成,细胞收缩和磷脂酰丝氨酸平行-接触。

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