Pyrogallol, a polyphenolic component of Acacia nilotica has previously been reported to induce apoptosis of diverse cell types. Pyrogallol is in part effective by influencing gene expression and by interference with mitochondrial function. Despite lack of nuclei and mitochondria, erythrocytes may undergo eryptosis, a suicidal death apparent from phosphatidylserine translocation to the erythrocyte surface and cell shrinkage. Eryptosis is triggered by glucose depletion, by oxidation, by hyperosmotic cell shrinkage and by excessive Ca²⁺ entry. As enhanced eryptosis is a common cause of anemia, uncovering inhibitors and stimulators of eryptosis may, both, be of clinical interest. Here we tested, whether eryptosis of human erythrocytes is modified by pyrogallol. Utilizing flow cytometry, phosphatidylserine abundance at the cell surface was estimated from annexin-V-binding and cell volume from forward scatter. Prior to determinations erythrocytes were incubated with or without glucose, without or with added oxidant tert-butyl-hydroperoxide (t-BOOH, 0.5 mM), without or with added hyperosmotic sucrose (550 mM) or without or with added Ca²⁺ ionophore ionomycin (1 µM). Treatment of erythrocytes with pyrogallol (2–8 µM) was without significant effect on annexin-V-binding and forward scatter. Glucose deprivation, t-BOOH, sucrose and ionomycin, each, triggered annexin-V-binding and decreased forward scatter. Pyrogallol significantly blunted the effects on annexin-V-binding but not on forward scatter. Pyrogallol thus blunts phosphatidylserine translocation in erythrocytes exposed to glucose depletion, oxidative stress, hyperosmotic shock and excessive Ca²⁺ entry.

邻苯三酚是尼古拉相思树的多酚成分，先前已报道其诱导多种细胞类型的细胞凋亡。邻苯三酚通过影响基因表达和干扰线粒体功能而部分有效。尽管缺乏细胞核和线粒体，但红细胞仍可能发生加密作用，这是由于磷脂酰丝氨酸易位至红细胞表面和细胞皱缩而导致的自杀死亡。葡萄糖的消耗，氧化，高渗细胞的收缩以及过量的Ca ²⁺触发了加密。条目。由于增强的加密作用是贫血的常见原因，因此揭露的抑制作用和刺激剂可能都具有临床意义。在这里，我们测试了邻苯三酚是否能修饰人红细胞的密码。利用流式细胞仪，从膜联蛋白-V-结合和从向前散射的细胞体积估计细胞表面的磷脂酰丝氨酸丰度。在测定前，将红细胞与葡萄糖一起或不与葡萄糖一起孵育，或不将氧化剂叔丁基氢过氧化物（t - BOOH，0.5 mM）加入，将高渗蔗糖（550 mM）加入或不加入或将Ca ²⁺添加或加入离子载体离子霉素（1 µM）。用邻苯三酚（2-8 µM）处理红细胞对膜联蛋白-V结合和前向散射无明显影响。葡萄糖剥夺，t -BOOH，蔗糖和离子霉素各引发膜联蛋白-V结合并降低前向散射。邻苯三酚显着减弱了对膜联蛋白V结合的影响，但对前向散射没有影响。因此，邻苯三酚会钝化暴露于葡萄糖耗竭，氧化应激，高渗性休克和过多Ca ²⁺进入的红细胞中的磷脂酰丝氨酸转运。