Irbesartan attenuates TNF-α-induced ICAM-1, VCAM-1, and E-selectin expression through suppression of NF-κB pathway in HUVECs

OBJECTIVE: It is widely recognized that atherosclerosis is a chronic inflammatory disease. Intracellular adhesion molecule-1 (ICAM-1), vascular cellular adhesion molecule-1 (VCAM-1), and E-selectin play vital roles in inflammatory processes. ICAM-1, VCAM-1, and E-selectin expression is regulated by nuclear factor (NF)-kappa B signaling. It has been reported that irbesartan can decrease expression of atrial fibrillation-Induced atrial adhesion molecule and reduce secretion of inflammation associated cytokines from cultured human carotid atheroma. In this study, we examined whether irbesartan prevents TNF-alpha-induced ICAM-1, VCAM-1, and E-selectin expression in human umbilical vein endothelial cells (HUVECs). MATERIALS AND METHODS: HUVECs were cultured. The expression of ICAM-1, VCAM-1 and MCP-1 was measured by real-time quantitative PCR and ELISA. The expression of NF-kappa B and p-I kappa B-alpha was measured by Western blot. RESULTS: It indicated that in HUVECs irbesartan inhibited expression and secretion of TNF alpha-induced ICAM-1, VCAM-1, and E-selectin. Furthermore, irbesartan inhibited TNF-alpha-induced I kappa B-alpha phosphorylation and NF-kappa B P65 nuclear translocation substantially. In conclusion, irbesartan attenuates TNF alpha-induced ICAM-1, VCAM-1, and E-selectin expression by way of suppressing the NF-kappa B pathways in HUVECs. Irbesartan might postpone the progression of inflammatory diseases, including atherosclerosis. CONCLUSIONS: Irbesartan attenuates TNF alpha-induced ICAM-1, VCAM-1 and MCP-1 expression through the suppression of NF-kappa B pathways. These results suggest irbesartan would be of great benefit to delaying the progression of inflammatory diseases, including atherosclerosis.