Endothelial adhesion plays an important role in the process of
atherosclerosis, which is regulated by endothelial adhesion molecules and
chemoattractant molecules. In some areas of China,
citreoviridin (
CIT) is considered a risk factor for the development of
atherosclerosis. Here, we investigated the role of
CIT in adhesion of human umbilical vein endothelial cells (HUVECs) together with the stimulation of
tumor necrosis factor-α (TNF-α). Adhesion of HUVECs to monocytes was analyzed by coculture experiments using U937 cells labeled with 2,7-bis(2-carboxyethyl)-5(6)-carboxyfluorescein acetoxymethylester. The expression of
intercellular adhesion molecule-1 (ICAM-1),
vascular cell adhesion molecule-1 (VCAM-1), and
E-selectin was determined by Western blot and
enzyme-linked
immunosorbent assay (ELISA). The expression of
monocyte chemoattractant protein-1 (MCP-1) was measured by reverse transcription polymerase chain reaction and ELISA. The activation of nuclear factor-κB (NF-κB) was assessed by Western blot and immunofluorescence staining.
CIT markedly increased TNF-α-induced HUVECs adhesion to monocytes and the expression levels of
ICAM-1,
VCAM-1,
E-selectin, and MCP-1. TNF-α-induced nuclear translocation of NF-κB in HUVECs was significantly elevated by
CIT. Our study demonstrates that
CIT upregulates TNF-α-induced endothelial adhesion via increasing activation of NF-κB, which results in the expression of
ICAM-1,
VCAM-1,
E-selectin, and MCP-1.
CIT plays a pivotal role in the process of endothelial cell adhesion and may thereby play an important role in the improvement of
atherosclerosis in areas of China that have a high prevalence of
CIT contamination and
atherosclerosis.