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Phlorhizin Protects against Erythrocyte Cell Membrane Scrambling

机译:Phlorhizin可以防止红细胞膜混乱

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Phlorhizin interferes with glucose transport. Glucose depletion triggers suicidal erythrocyte death or eryptosis, characterized by cell shrinkage and cell membrane scrambling. Eryptosis is further triggered by oxidative stress. The present study explored whether phlorhizin influences eryptosis following glucose depletion or oxidative stress. Cell membrane scrambling was estimated from annexin binding, cell volume from forward scatter (FSC), and cytosolic Cat{ concentration from Fluo-3 fluorescence. Phlorhizin (10-100 μM) added alone did not modify scrambling, FSC, or Fluo-3 fluorescence. Glucose depletion (48 h) significantly increased Fluo-3 fluorescence, decreased FSC, and increased annexin binding, effects in part significantly blunted by phlorhizin (annexin binding ≥10 μM, FSC≥ 50 μM). Oxidative stress (30 min 0.3 mM tert-butylhydroperoxide) again significantly increased Fluo-3 fluorescence and triggered annexin binding, effects again in part significantly blunted by phlorhizin (Fluo-3 fluorescence ≥ 50 μM, annexin-binding ≥ 10μM). Phlorhizin did not blunt the cell shrinkage induced by oxidative stress. The present observations disclose a novel effect of phlorhizin, that is, an influence on suicidal erythrocyte death following energy depletion and oxidative stress.
机译:磷霉素可干扰葡萄糖的转运。葡萄糖耗竭触发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。氧化应激进一步触发了加密。本研究探讨了Phlorhizin是否会影响葡萄糖耗尽或氧化应激后的隐匿性。从膜联蛋白结合,从前向散射(FSC)的细胞体积和从Fluo-3荧光得到的胞质Cat {浓度”估计细胞膜的扰乱。单独添加的磷霉素(10-100μM)不会改变加扰,FSC或Fluo-3荧光。葡萄糖耗竭(48小时)显着增加了Fluo-3荧光,降低了FSC,并增加了膜联蛋白结合,其效果在一定程度上被发磷菌素减弱了(annexin结合≥10μM,FSC≥50μM)。氧化应激(30分钟,0.3 mM叔丁基氢过氧化物)再次显着增加了Fluo-3荧光并触发了膜联蛋白的结合,再次部分受到了磷霉素的影响(Fluo-3荧光≥50μM,膜联蛋白结合≥10μM)。磷霉素没有抑制氧化应激诱导的细胞收缩。目前的观察结果揭示了Phlorhizin的新作用,即对能量消耗和氧化应激后自杀性红细胞死亡的影响。

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