首页> 外文期刊>Life sciences >Genistein attenuates D-galactose-induced oxidative damage through decreased reactive oxygen species and NF-kappaB binding activity in neuronal PC12 cells.
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Genistein attenuates D-galactose-induced oxidative damage through decreased reactive oxygen species and NF-kappaB binding activity in neuronal PC12 cells.

机译:金雀异黄素通过减少神经细胞PC12细胞中的活性氧和NF-κB的结合活性来减轻D-半乳糖诱导的氧化损伤。

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AIMS: We investigated the mechanism of D-galactose (DG)-induced oxidative damage and the neuroprotective action of genistein in PC12 cells. MAIN METHODS: PC12 cells were treated with 40mM DG dissolved in medium containing 85% RPMI1640, 10% HBS and 5% FBS with or without genistein. We measured the protein expression of beta-amyloid (Abeta), advanced glycation end products (AGEs), IkappaB-alpha and manganese-superoxide dismutase (MnSOD) by western blotting, intracellular reactive oxygen species (ROS) by 2, 7-dichlorofluorescin-diacetate, and the binding activity of nuclear factor kappa B (NF-kappaB) by electrophortic mobility shift assay. KEY FINDINGS: DG (40mM) completely retarded cell growth after incubation for 72h, and this effect was not due to osmotic changes, as 40mM mannitol had no effect. Mechanistically, we found that DG increased intracellular ROS starting at 4h and increased Abeta and AGEs at 24h. DG treatment for 24h also increased the binding activity of NF-kappaB but strongly decreased the expression of IkappaB-alpha protein. Furthermore, DG treatment for 48h increased MnSOD protein expression. All these effects of DG were effectively inhibited by genistein (0.5-10muM). SIGNIFICANCE: The present study indicates that the protection of genistein against DG-induced oxidative stress in PC12 cells, and the effect is likely mediated by decreased intracellular ROS and binding activity of NF-kappaB.
机译:目的:我们研究了D-半乳糖(DG)引起的氧化损伤的机理以及染料木黄酮对PC12细胞的神经保护作用。主要方法:PC12细胞用溶解于含有85%RPMI1640、10%HBS和5%FBS的含或不含染料木黄酮的培养基中的40mM DG处理。我们通过Western blotting,2,7-dichlorofluorescin-通过电泳迁移率变动分析确定双乙酸盐和核因子κB(NF-κB)的结合活性。主要发现:DG(40mM)在温育72h后完全延迟了细胞生长,并且这种作用不是由于渗透变化,因为40mM甘露醇没有作用。从机理上讲,我们发现DG从4h开始增加细胞内ROS,并在24h增加Abeta和AGEs。 DG处理24h还增加了NF-kappaB的结合活性,但强烈降低了IkappaB-α蛋白的表达。此外,DG处理48h可增加MnSOD蛋白表达。染料木黄酮(0.5-10μM)可有效抑制DG的所有这些作用。意义:本研究表明,染料木黄酮可以保护PC12细胞免受DG诱导的氧化应激,其作用可能是由细胞内ROS的减少和NF-κB的结合活性介导的。

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