Selenium Nanoparticles Inhibited H2O2-Induced Endothelial Cell Dysfunction by Alleviating Oxidative Stress.

Abstract

Endothelial dysfunction is one of the important pathological bases of atherosclerosis, and cardiovascular diseases caused by atherosclerosis are the first major cause of human death. Our previous studies indicated that selenium nanoparticles (SeNPs) could prevent experimental atherosclerosis in animals, while their association with endothelial dysfunction remain unclear. Meanwhile, the size and surface properties of nanomaterials have a great influence on their biological functions. In this study, we prepared SeNPs with different sizes and surface charges to study their effects on H₂O₂-induced endothelial dysfunction in endothelial cells and the possible mechanisms. The results showed that SeNPs pretreatment significantly reduced the endothelial cell injury and dysfunction caused by H₂O₂. SeNPs pretreatment also significantly inhibited H₂O₂-induced oxidative stress, probably by enhancing cellular Se content and antioxidant selenoprotein expression in endothelial cells. Additionally, SeNPs pretreatment reversed H₂O₂-induced changes of Nrf2/Keap1 pathway. Moreover, SeNPs with middle size (around 40 nm) exhibited advantage in increasing cellular Se uptake and expression of antioxidant selenoproteins compared with smaller size (around 20 nm) or larger size (around 80 nm). Overall, SeNPs protect endothelial cells from H₂O₂-induced endothelial dysfunction by alleviating oxidative stress, and this activity may be dependent on their particle size. These results provided a deeper understanding of the anti-endothelial dysfunction activity of SeNPs and contribute to the potential use of SeNPs as a therapeutic agent against atherosclerosis in the future.