CS-SeNPs and Na2SeO3 suppressed endothelial NF-κB activation and, subsequently, target gene expression, including adhesion molecules VCAM-1, E-selectin and ICAM-1, chemokine MCP-1, cytokines TNF-α, IL-6 and IL-1β, pro-inflammatory molecule iNOS, leading to decreased endothelial dysfunction and inflammatory response. The gene discussed is NFKB1; the disease is endothelial dysfunction.