The apoptosis induced by silica nanoparticle through endoplasmic reticulum stress response in human pulmonary alveolar epithelial cells.

Recently, the use of silica nanoparticles (SiO-NPs) and mesoporous silica nanoparticles (mSiO-NPs) in the biomedical field, such as biosensors, drug deliveries and bioactivator carriers, is increasing due to their special physiochemical properties. However, the biosafety assessment of them is far lagging behind their rapid application. In this study, we observed that both SiO-NPs and mSiO-NPs with certain exposed doses decreased the cell viability while increased the apoptosis rates in the human pulmonary alveolar epithelial cells (HPAEpiC). Generally, mSiO-NPs presented less toxic effects than SiO-NPs with same treated dose, which assures the positive application prospect of mSiO-NPs in the area of biomedicine. Since both SiO-NPs could be taken into cells and accumulated in the endoplasmic reticulum (ER), which resulted in pathologically morphological changes and subcellular organelle damages, we hypothesized that the ER stress response could be involved in the NPs-induced apoptosis. The findings suggested that SiO-NPs and mSiO-NPs exposure increased the expression levels of two ER stress markers, e.g. BiP and CHOP, which could be inhibited by the ER stress inhibitor 4-PBA, following with decreased apoptosis rates in HPAEpiC. Even though it is still unclear of the direct target of NPs causing ER stress response following with cell apoptosis, our findings provide a novel insight for researchers to explore the toxic mechanisms of SiO-NPs and mSiO-NPs in order to reduce the adverse effects of them.