【摘 要】
：
With application of nano-sized silica-containing particles (Nano-Si) expanding, the health concerns about their adverse effects on the pulmonary systemare increasing.However, the mechanisms for the pu
【机 构】
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School of Public Health, Capital Medical University, Beijing, 100069, P.R.China; Beijing Key Laborat
【出 处】
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首都医科大学公共卫生学院第四届研究生学术论坛
论文部分内容阅读
With application of nano-sized silica-containing particles (Nano-Si) expanding, the health concerns about their adverse effects on the pulmonary systemare increasing.However, the mechanisms for the pulmonary toxicity of these materials remain unclear.In the present study, we focused on the impacts of silica nanoparticles (SNPs) on dna methylation, a AKT-dependent deacetylase, and investigated whether BCL-2 was involved in SNPs induced apoptosis.The SNPs tended to entered into the human bronchial epithelial cells (BEAS-2B) and released Si2+ inside the cells.SNPs at doses of 5μg/ML for 30 passages inhibited the cell viability.SNPs produced cytotoxicity was demonstrated through an apoptotic process, indicated by increased the caspase-3activation.The DNA BCL-2 and CREB were hypermethylation ,and the expression of BCL-2 and CREB was markedly down-regulated by the SNPs, accompanied by the influence of AKT.Our results suggest that the repression of BCL-2 and CREB may underlie the SNPs-induced apoptosis via PI3K/Akt/CREB signaling pathway.This knowledge of the impact of SNPs on BCL-2 and CREB may lead to an improved understanding of the toxic mechanisms of Nano-Si and provide a molecular target to antagonize Nano-Si toxicity.
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