Natural flavone tricetin suppresses oxidized LDL-induced endothelial inflammation mediated by Egr-1

•Tricetin prevented ox-LDL- induced expression of MCP-1, IL-1β and generation of ROS.•Tricetin inhibited attachment of U937 monocytes to HUVECs by ICAM-1 and VCAM-1.•Tricetin reduced ox-LDL- induced endothelial inflammation by inhibiting LOX-1/ERK1/2/Egr-1. Atherosclerosis is the primary cause of many cardiovascular diseases. Endothelial dysfunction is recognized as a crucial early event in atherosclerotic lesion formation. Tricetin is a natural flavonoid derivative that has demonstrated a wide range of therapeutic properties. This study investigates the protective effect of tricetin in cultured endothelial cells. The results of our study show that tricetin suppressed oxidized low-density lipoprotein (ox-LDL)-induced expression of pro-inflammatory monocyte chemotactic protein-1 (MCP-1) and interleukin-1β (IL-1β), as well as the generation of reactive oxygen species (ROS). Furthermore, our findings indicate that tricetin suppressed ox-LDL-induced expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). At the cellular level, the presence of tricetin inhibited ox-LDL-induced monocyte adhesion to endothelial cells. Mechanistically, we showed that tricetin suppressed the induction of the endothelial receptor for ox-LDL, lectin-like ox-LDL receptor-1 (LOX-1), and the transcriptional factor early growth response 1 (Egr-1) as well as extracellular signal-regulated protein kinase 1 and 2 (ERK1/2) activation. These data demonstrate that tricetin is a natural protective agent in vascular endothelial cells, indicating that tricetin could have a potentially beneficial effect in the modulation of atherosclerosis.