The transcriptional nuclear factor (NF)-B can be activated by diverse stimuli such as cytokines, mittens, oxidative stress, and lipids, leading to the transactivation of several genes that play important roles in the development of vascular diseases. A key step in the inflammatory response is adhesion of leukocytes to endothelial cells lining the blood vessels, with subsequent extravasation of the leukocytes into the involved tissue. Because high glucose may play a key role in the pathogenesis of diabetic vascular disease, we have examined whether culture of human umbilical vein endothelial cells (HUVECs) under high glucose (HG) condition (30 mmol/L) can lead to die activation of NF-B, and also whether E-selectin expression and neutrophil adhesion and migration were altered by HG culture. We observed that HUVECs cultured in HG showed significantly greater activation of NF-B in the basal state compared with cells cultured in normal glucose (NG) (5.5 mmol/L). The expression of E-selectin was increased incubated with HG compared with NG. Coculture of neutrophils and HUVECs under HG showed a significant increase in the adhesion of neutrophil to monolayer of HUVECs and stimulation of migration of neutrophil across cultured endothelial monolayers. HUVECs are stimulated by HG to express E-selectin, which interact with carbohydrate ligands on leukocytes through activation of NF-B. These results suggest that hyperglycemia-induced acdvation of NF-B in HUVECs may be a key mechanism for the accelerated vascular disease observed in diabetes.