首页> 美国卫生研究院文献>American Journal of Physiology - Cell Physiology >Cell Signaling: Proteins Pathways and Mechanisms: Nonlethal dose of silver nanoparticles attenuates TNF-α-induced hepatic epithelial cell death through HSP70 overexpression
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Cell Signaling: Proteins Pathways and Mechanisms: Nonlethal dose of silver nanoparticles attenuates TNF-α-induced hepatic epithelial cell death through HSP70 overexpression

机译:细胞信号传导:蛋白质途径和机制:非致死剂量的银纳米颗粒通过HSP70过表达减轻TNF-α诱导的肝上皮细胞死亡

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摘要

Silver nanoparticles (Ag-nps) have been widely used in various biomedical products. Compared with its hazardous effects extensively being studied, rare attention has been paid to the potential protective effect of Ag-nps to human health. The present study was designed to evaluate the protective effects of Ag-nps and heat shock treatment on tumor necrosis factor-α (TNF-α)-induced cell damage in Clone 9 cells. Clone 9 cells were pretreated with nonlethal concentration of Ag-nps (1 μg/ml) or heat shock, and then cell damages were induced by TNF-α (1 ng/ml). Protective effects of Ag-nps administration or heat shock treatment were determined by examining the TNF-α-induced changes in cell viabilities. The results showed that the intensity of cytotoxicity produced by TNF-α was alleviated upon treatment with nonlethal concentration of Ag-nps (1 μg/ml). Similar protective effects were also found upon heat shock treatment. These data demonstrate that Ag-nps and heat shock treatment were equally capable of inducing heat shock protein 70 (HSP70) protein expression in Clone 9 cells. The results suggest that clinically Ag-nps administration is a viable strategy to induce endogenous HSP70 expression instead of applying heat shock. In conclusion, our study for the first time provides evidence that Ag-nps may act as a viable alternative for HSP70 induction clinically.
机译:银纳米颗粒(Ag-nps)已广泛用于各种生物医学产品中。与其广泛研究的危害作用相比,人们很少关注Ag-nps对人体健康的潜在保护作用。本研究旨在评估Ag-nps和热休克治疗对Clone 9细胞中肿瘤坏死因子-α(TNF-α)诱导的细胞损伤的保护作用。用非致死浓度的Ag-nps(1μg/ ml)或热休克预处理克隆9细胞,然后由TNF-α(1 ng / ml)诱导细胞损伤。通过检查TNF-α诱导的细胞活力变化来确定施用Ag-nps或热休克治疗的保护作用。结果表明,用非致死浓度的Ag-nps(1μg/ ml)处理后,TNF-α产生的细胞毒性强度得到缓解。在热激处理中也发现了类似的保护作用。这些数据表明,Ag-nps和热休克处理同等能力能够诱导克隆9细胞中的热休克蛋白70(HSP70)蛋白表达。结果表明,临床上Ag-nps给药是诱导内源性HSP70表达而不是施加热激的可行策略。总之,我们的研究首次提供了证据,表明Ag-nps可能在临床上可作为HSP70诱导的可行替代方法。

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