Effect of prostaglandin E1 on TNF-induced vascular inflammation in human umbilical vein endothelial cells

Prostaglandin E-1 (PGE(1)) is a member of the prostaglandins and has a variety of cardiovascular protective effects. Increasing attention has been paid to the anti-inflammation activity of PGE(1), but little direct evidence has been found. We investigated the effects of PGE(1) on cell adhesion and inflammation and the mechanisms responsible for this activity in tumor necrosis factor (TNF)-treated human umbilical vein endothelial cells. Results demonstrated that pretreatment with PGE(1) decreased the adhesion between vascular endothelial cells and monocytes, reduced the expression of vascular cell adhesion molecule-1, intercellular adhesion molecule-1, and E-selectin in vascular endothelial cells. In addition, PGE(1) suppressed TNF-induced NF-kappa B activation and production of reactive oxygen species. We concluded that PGE(1) suppressed the vascular inflammatory process, which might be closely related to the inhibition of reactive oxygen species and NF-kappa B activation in human umbilical vein endothelial cells.