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A Critical Role of Redox State in Determining HL-60 Cell Differentiation

机译:氧化还原状态在确定HL-60细胞分化中的关键作用

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The modifications of intracellular redox balance leads to important cellular changes in many cell types. Here, a causal relationship between redox state and monocytic differentiation induced by isoliquiritigennin(ISL) have been studied in the human acute promyelocytic leukaemia HL-60 cells. The modulations of intracellular reactive oxygen species levels by D, L-buthionine-(S, R) sulfoximide (BSO), and N-acetyl-L-cysteine (NAC) caused inducer- and time-dependent or stage-specific effects on HL-60 cell growth inhibition and differentiation. ISL increased intracellular Superoxide anions (O2~(·-)) that was completely inhibited by BSO and NAC. ISL increased NBT reduction ability and the expressions of surface antigens CD11b and CD14 were completely inhibited by BSO and NAC. These observations suggest a critical role of redox state in determining HL-60 cell behaviour and provide new insights into the complex effects of redox perturbations on the intracellular signalling network.
机译:细胞内氧化还原平衡的修饰导致许多细胞类型中的重要细胞变化。这里,已经在人急性突出细胞胶质细胞白血病HL-60细胞中研究了isoliquiritigenin(ISL)诱导的氧化还原状态和单核细胞分化之间的因果关系。 D,L-苯胺 - (S,R)磺酰胺(BSO)和N-乙酰基-1-半胱氨酸(NAC)对细胞内反应性氧物质水平的调节引起了对HL的诱导和时间依赖性或阶段特异性的影响-60细胞生长抑制和分化。 ISL含量增加通过BSO和NAC完全抑制的细胞内超氧化物阴离子(O 2〜(· - ))。 ISL增加了NBT还原能力,并通过BSO和NAC完全抑制了表面抗原CD11B和CD14的表达。这些观察结果表明氧化还原状态在确定HL-60细胞行为方面的关键作用,并为细胞内信令网络的氧化还原扰动的复杂效果提供新的见解。

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