The role of potassium channel in silica nanoparticle-induced inflammatory effect in human vascular endothelial cells in vitro.

Exposure to nanoparticles became popular in industry and daily life. Nano-SiO₂ was shown to have an adverse effect to vascular endothelial cell although the mechanisms remain unclear. To test whether the nano-SiO₂'s harmful effect was related to the potassium channel, human umbilical vascular endothelial cells (HUVECs) were treated with nano-SiO₂ in different dose. Cell survival rate and lactate dehydrogenase (LDH) as cytotoxic parameters, tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) as inflammation indicators were determined. The electrophysiological changes and function of potassium channel were detected with patch clamp and channel blockers. It was found that nano-SiO₂ exposure decreased cell survival rate, increased LDH leakage, TNF-α and IL-6 production. The potassium channel activity was increased in the opening rate and current intensity. Furthermore, potassium channel blockers tetraethylammonium (TEA), 4-amino pyridine (4-AP), and margatoxin (MGTX) reduced the nano-SiO₂-induced cytotoxity and inflammation, i.e., increase in the cell survival rate, and decrease in the LDH leakage and production of TNF-α and IL-6. It might be concluded that the nano-SiO₂-induced inflammation and cytotoxicity at HUVECs was associated with the activation of potassium channel.