Selenium nanoparticles attenuate retinal pathological angiogenesis by disrupting cell cycle distribution

This study aims to explore the mechanism by which selenium nanoparticles (SeNPs) inhibit retinal neovascularization (RNV) and to identify a more effective treatment for pathological RNV. The characterization and identification of the synthesized selenium nanoparticles (SeNPs) were conducted to investigate their effects on the function of human umbilical vein endothelial cells (HUVECs), retinal blood vessel development in mice, and the impact on oxygen-induced retinopathy. Tritium-labeled thymine was utilized to label newly synthesized DNA both in vivo and in vitro, allowing for the observation of SeNPs' effects on cell proliferation. Additionally, flow cytometry, immunofluorescence, and western blotting techniques were employed to elucidate the mechanisms by which SeNPs inhibit retinal neovascularization. SeNPs can significantly inhibit the functions of vascular endothelial cells, particularly their proliferation, both in vivo and in vitro. The SeNPs achieve this by modulating the expression of cell cycle-related proteins through the regulation of the PI3K-AKT-p21 axis, which in turn inhibits the transition of the cell cycle from the G1 phase to the S phase. SeNPs may be a novel treatment for the interference of retinal neovascularization.