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.
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.
Authors: Young Min Ham; Hae Seong Song; Jeong Eun Kwon; Hyelin Jeon; Hyun Jin Baek; Chang Won Kim; Weon-Jong Yoon; Eui Su Choung; Se Chan Kang Journal: J Nat Med Date: 2018-07-31 Impact factor: 2.343
Authors: Nancy Buechler; Xianfeng Wang; Barbara K Yoza; Charles E McCall; Vidula Vachharajani Journal: J Immunol Res Date: 2017-04-19 Impact factor: 4.818