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

Y. Jiang, L.-L.I. Jiang, X.-M.Z.Y. Maimaitirexiati, Y. Zhang, L. Wu

Intensive Care Unit, Tumor Hospital Affiliated to Xinjiang Medical University, Urumqi, China. wulixj@163.com

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• Pharmacology

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)-κB 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-α-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-κB and p-IκB-α was measured by Western blot.

RESULTS: It indicated that in HUVECs irbesartan inhibited expression and secretion of TNFα-induced ICAM-1, VCAM-1, and E-selectin. Furthermore, irbesartan inhibited TNF-α-induced IκB-α phosphorylation and NF-κB P65 nuclear translocation substantially. In conclusion, irbesartan attenuates TNFα-induced ICAM-1, VCAM-1, and E-selectin expression by way of suppressing the NF-κB pathways in HUVECs. Irbesartan might postpone the progression of inflammatory diseases, including atherosclerosis.

CONCLUSIONS: Irbesartan attenuates TNFα-induced ICAM-1, VCAM-1 and MCP-1 expression through the suppression of NF-κB pathways. These results suggest irbesartan would be of great benefit to delaying the progression of inflammatory diseases, including atherosclerosis.

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