Effect of 2-TeCD on the expression of adhesion molecules in human umbilical vein endothelial cells under the stimulation of tumor necrosis factor-alpha.

Adhesion molecules play an important role in the pathogenesis of atherogenesis. They are expressed on endothelial cells surface in response to various inflammatory stimuli. In this paper, we examined the effect of 2-tellurium-bridged beta-cyclodextrin (2-TeCD), a GPx mimic, on the expression of adhesion molecules in human umbilical vein endothelial cells (HUVECs) under tumor necrosis factor-alpha (TNF-alpha) stimulation. Experimental results indicated that 2-TeCD suppressed the TNF-alpha-induced the expression of vascular adhesion molecule-1 (VCAM-1) and intercellular cell adhesion molecule-1 (ICAM-1) on HUVECs surface in a dose-dependent manner. 2-TeCD also reduced the level of mRNA expression of VCAM-1 and ICAM-1. Furthermore, 2-TeCD inhibited THP-1 monocyte adhesion to HUVECs stimulated by TNF-alpha. Nuclear factor-kappaB (NF-kappaB) could regulate transcription of VCAM-1 and ICAM-1 genes. Western blot analysis showed that 2-TeCD inhibited the translocation of the p65 subunit of NF-kappaB into the nucleus. In short, these results indicated that 2-TeCD inhibits TNF-alpha-stimulated VCAM-1 and ICAM-1 expression in HUVECs partly due to suppressing translocation of NF-kappaB.