Tripterine inhibits the expression of adhesion molecules in activated endothelial cells

• DOI: 10.1189/jlb.1005611
• Publication Date: 2006-06-13T00:46:01Z
• Authors: Deng-hai Zhang; Anthony Marconi; Li-min Xu; Chun-xin Yang; Guo-wu Sun; Xiao-ling Feng; Chang-quan Ling; Wan-zhang Qin; Georges Uzan; Patrizia d’Alessio
• Keywords: Proinflammatory cytokine; VCAM-1

Abstract Cell adhesion molecules (CAM) expressed by vascular endothelium in response to cytokine stimulation play a key role leukocyte during the inflammatory response. Tripterine, chemical compound of Chinese plant Tripterygium wilfordii Hook f, displays anti-inflammatory properties several animal models. However, mechanisms its action are poorly understood. In present study, we show that conditions, mimicked tumor necrosis factor α (TNF-α) stimulation, pretreatment for 6 h with tripterine at nontoxic concentrations 20–200 nM inhibits expression E-selectin, cell molecule (CAM)-1 (VCAM-1), and intercellular molecule-1 (ICAM-1) human umbilical vein endothelial cells (HUVEC) dose-dependent manner. Tripterine (200 nM) almost completely VCAM-1 [50% inhibitory concentration (IC50)=52 nM] ICAM-1 (IC50=51 73% E-selectin (IC50=94 nM). This inhibition effect is prominent, compared dexamethasone, ibuprofen, methotrexate, or probucol, which revealed much weaker doses as high 1 mM. Effects on CAM other proinflammatory cytokines, such interleukin-1β interferon-γ, were also inhibited significantly tripterine. Moreover, significant was equally observable postincubation experiments. addition, monocytes T lymphocytes TNF-α-stimulated HUVEC. Finally, TNF-α-driven mRNA transcription nuclear factor-κB (NF-κB) translocation. Hence, describe new mechanism tripterine’s obtained nanomolar concentrations, owing negative regulation cytokine-induced adhesiveness endothelium.