title: Irbesartan attenuates TNF-α-induced ICAM-1, VCAM-1, and E-selectin expression through suppression of NF-κB pathway in HUVECs.
abstract: 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).
  
  
  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.affiliation: Intensive Care Unit, Tumor Hospital Affiliated to Xinjiang Medical University, Urumqi, China. wulixj@163.com.
authors.forename: Y
authors.initials: Y
authors.lastname: Jiang
authors.forename: L-L I
authors.initials: LL
authors.lastname: Jiang
authors.forename: X-M Z Y
authors.initials: XM
authors.lastname: Maimaitirexiati
authors.forename: Y
authors.initials: Y
authors.lastname: Zhang
authors.forename: L
authors.initials: L
authors.lastname: Wu
mesh_terms: D050197:Atherosclerosis / Q000378:metabolism*; D001713:Biphenyl Compounds / Q000494:pharmacology / Q000627:therapeutic use*; D061307:Human Umbilical Vein Endothelial Cells / Q000166:cytology / Q000378:metabolism*; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism*; D000077405:Irbesartan; D016328:NF-kappa B / Q000378:metabolism*; D015398:Signal Transduction; D013777:Tetrazoles / Q000494:pharmacology / Q000627:therapeutic use*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism*
chemical_list: D001713:Biphenyl Compounds; D016328:NF-kappa B; D013777:Tetrazoles; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D000077405:Irbesartan