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首页> 外文期刊>Cellular Physiology and Biochemistry >Stimulation of Suicidal Erythrocyte Death by Artesunate
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Stimulation of Suicidal Erythrocyte Death by Artesunate

机译：青蒿琥酯刺激自杀性红细胞死亡

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biBackground /i/bThe artemisinin derivative artesunate is effective in the treatment of severe malaria and is considered for the treatment of malignancy. Artesunate triggers tumor cell apoptosis, an effect at least in part mediated by mitochondria. Even though lacking mitochondria, erythrocytes may similarly enter suicidal death or eryptosis, which is characterized by cell shrinkage and breakdown of the phospholipid asymmetry of the cell membrane with phosphatidylserine translocation to the erythrocyte surface. Triggers of eryptosis include increase of cytosolic Casup2+/sup-activity ([Casup2+/sup]subi/sub), ceramide formation, and oxidative stress. The present study explored whether artesunate stimulates eryptosis. biMethods /i/bPhosphatidylserine exposure at the cell surface was estimated from annexin V binding, cell volume from forward scatter, [Casup2+/sup]subi/sub from Fluo3-fluorescence, ceramide abundance from binding of specific antibodies, and oxidative stress from 2′,7′-dichlorodihydrofluorescein-diacetate fluorescence. biResults /i/bA 48 h exposure of human erythrocytes to artesunate significantly increased the percentage of annexin-V-binding cells (≥ 9 µg/ml) without significantly influencing forward scatter. Artesunate significantly increased [Casup2+/sup]subi/sub. The stimulation of annexin-V-binding by artesunate (15 µg/ml) was significantly blunted but not abolished by removal of extracellular Casup2+/sup. Artesunate increased the ceramide abundance at the cell surface and the 2′,7′-dichlorodihydrofluorescein-diacetate fluorescence. biConclusions /i/bArtesunate stimulates phosphatidylserine translocation at the erythrocyte cell membrane, an effect at least partially due to increase of [Casup2+/sup]subi/sub, stimulation of ceramide formation and generation of oxidative stress.
机译：背景 青蒿素衍生物青蒿琥酯可有效治疗严重疟疾，并被认为可治疗恶性肿瘤。青蒿琥酯触发肿瘤细胞凋亡，这种作用至少部分由线粒体介导。即使缺乏线粒体，红细胞也可能类似地进入自杀死亡或隐匿性死亡，其特征是细胞收缩和磷脂酰丝氨酸易位至红细胞表面的细胞膜磷脂不对称性破裂。加密的触发因素包括胞质Ca 2 + -活性（[Ca 2 + ] i ）的增加，神经酰胺的形成和氧化应激。本研究探讨了青蒿琥酯是否刺激隐匿性。 方法 根据膜联蛋白V结合，正向散射的细胞量，[Ca 2 + ] i估算细胞表面的磷脂酰丝氨酸暴露量来自Fluo3-荧光，来自特定抗体结合的神经酰胺丰度，以及来自2'，7'-dichlorodihydrofluorescein-diacetate荧光的氧化应激。 结果 人红细胞暴露于青蒿琥酯48小时可显着增加膜联蛋白V结合细胞（≥9 µg / ml）的百分比，而不会显着影响前向散射。青蒿琥酯显着增加[Ca 2 + ] i 。青蒿琥酯（15 µg / ml）对膜联蛋白-V结合的刺激作用明显减弱，但去除细胞外Ca 2 + 并没有消除。青蒿琥酯可增加细胞表面神经酰胺的丰度，并增加2'，7'-二氯二氢荧光素-二乙酸酯的荧光。 结论 青蒿琥酯刺激磷脂酰丝氨酸在红细胞膜上的移位，这种作用至少部分是由于[Ca 2 + ] i的增加，刺激神经酰胺的形成和氧化应激的产生。

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