首页> 外文期刊>American Journal of Physiology >CALL FOR PAPERS I Cell Signaling: Proteins, Pathways and Mechanisms Nonlethal dose of silver nanoparticles attenuates TNF-a-induced hepatic epithelial cell death through HSP70 overexpression
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CALL FOR PAPERS I Cell Signaling: Proteins, Pathways and Mechanisms Nonlethal dose of silver nanoparticles attenuates TNF-a-induced hepatic epithelial cell death through HSP70 overexpression

机译:呼吁纸张I细胞信号传导:蛋白质,途径和机制无血栓剂剂量银纳米粒子通过Hsp70过表达衰减TNF-A诱导的肝上皮细胞死亡

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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-a (TNF-a)-induced cell damage in Clone 9 cells. Clone 9 cells were pretreated with nonlethal concentration of Ag-nps (1 |xg/ml) or heat shock, and then cell damages were induced by TNF-a (1 ng/ml). Protective effects of Ag-nps administration or heat shock treatment were determined by examining the TNF-a-induced changes in cell viabilities. The results showed that the intensity of cytotoxicity produced by TNF-a was alleviated upon treatment with nonlethal concentration of Ag-nps (1 (Jig/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:银纳米粒子(AG-NPS)已广泛用于各种生物医学产品。与广泛研究的危险效果相比,难以注意到AG-NP对人体健康的潜在保护作用。本研究旨在评估Ag-NPS和热休克治疗对肿瘤坏死因子-α(TNF-A)诱导的克隆9细胞损伤的保护作用。用非致力浓度的Ag-NPS(1 | Xg / ml)或热冲击预处理克隆9细胞,然后通过TNF-A(1ng / ml)诱导细胞损伤。通过检查细胞活性的TNF-A诱导的变化来确定AG-NPS给药或热休克治疗的保护作用。结果表明,在用非致力浓度的Ag-nps(1(夹具/ m​​l)处理时,通过TNF-A产生的细胞毒性强度。在热休克治疗时也发现了类似的保护作用。这些数据表明AG-NPS表明AG-NPS热休克治疗同样能够在克隆9细胞中诱导热休克蛋白70(HSP70)蛋白表达。结果表明,临床上Ag-NPS管理是诱导内源性HSP70表达而不是施加热冲击的可行策略。总结,我们首次进行的研究提供了证据,即AG-NPS可以临床上作为HSP70诱导的可行替代品。

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