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Silver nanoparticles induce p53-mediated apoptosis in human bronchial epithelial (BEAS-2B) cells

机译:银纳米颗粒诱导人支气管上皮(BEAS-2B)细胞中p53介导的凋亡

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Deregulated apoptosis has been associated with many lung diseases. Although many studies have reported the apoptotic effects exhibited by silver nanoparticles (Ag-NPs) in various circumstances, the apoptosis mechanism of Ag-NPs is unclear. We investigated oxidative stress and apoptosis in human normal bronchial epithelial (BEAS-2B) cells to elucidate the role of p53 in apoptosis by Ag-NPs. First, dispersion and stability of Ag-NPs improved using bronchial epithelial cell growth medium with 5% fetal bovine serum. Then, we observed oxidative stress in BEAS-2B cells exposed to Ag-NPs. Second, we carried out a cell death assay to measure DNA fragmentation as a biomarker of apoptosis. BEAS-2B cells were treated with p53-specific short interfering RNA (siRNA) or p53 inhibitor (pifithrin-α) to investigate whether p53 is involved in apoptosis by Ag-NPs. As a result, Ag-NPs significantly enhanced DNA fragmentation dose-dependently and treatment with p53 siRNA or pifithrin-α prevented DNA fragmentation. We also found that apoptosis-related genes (caspase-3, Bax, and Bcl-2) were regulated by Ag-NPs, which was detected by mRNA and protein levels. These results suggest that Ag-NPs induced p53-mediated apoptosis in BEAS-2B cells. Our findings may contribute to understanding the potential roles of Ag-NPs in pulmonary disease.
机译:细胞凋亡失调与许多肺部疾病有关。尽管许多研究报道了银纳米颗粒(Ag-NPs)在各种情况下均表现出凋亡作用,但Ag-NPs的凋亡机制尚不清楚。我们调查了人类正常支气管上皮(BEAS-2B)细胞中的氧化应激和凋亡,以阐明p-53在Ag-NPs凋亡中的作用。首先,使用含5%胎牛血清的支气管上皮细胞生长培养基可提高Ag-NP的分散性和稳定性。然后,我们观察到暴露于Ag-NPs的BEAS-2B细胞的氧化应激。其次,我们进行了细胞死亡测定,以测量DNA片段化作为凋亡的生物标记。用p53特异性短干扰RNA(siRNA)或p53抑制剂(pifithrin-α)处理BEAS-2B细胞,以研究p-53是否参与Ag-NP的凋亡。结果,Ag-NPs显着剂量依赖性地增强了DNA片段化,用p53 siRNA或pifithrin-α处理可防止DNA片段化。我们还发现,凋亡相关基因(caspase-3,Bax和Bcl-2)受Ag-NPs的调控,而Ag-NPs则由mRNA和蛋白质水平检测到。这些结果表明,Ag-NPs诱导BEAS-2B细胞中p53介导的凋亡。我们的发现可能有助于理解Ag-NP在肺部疾病中的潜在作用。

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