Pretreatment with Prostaglandin E1 decreased adhesion between vascular endothelial cells and monocytes and suppressed TNF-induced NF-kappaB activation and reactive oxygen species production.
Does Prostaglandin E1 reduce vascular inflammation in TNF-treated human umbilical vein endothelial cells?
PGE1 suppresses vascular inflammation in endothelial cells by inhibiting ROS production and NF-kappaB activation, providing mechanistic evidence for its cardiovascular protective effects.
Prostaglandin E1 (PGE1) 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 PGE1, but little direct evidence has been found. We investigated the effects of PGE1 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 PGE1 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, PGE1 suppressed TNF-induced NF-kappaB activation and production of reactive oxygen species. We concluded that PGE1 suppressed the vascular inflammatory process, which might be closely related to the inhibition of reactive oxygen species and NF-kappaB activation in human umbilical vein endothelial cells.
Fang et al. (Sat,) conducted a other in Vascular inflammation (in vitro). Prostaglandin E1 (PGE1) vs. TNF alone was evaluated on Cell adhesion, inflammation, and expression of adhesion molecules (VCAM-1, ICAM-1, E-selectin). Pretreatment with Prostaglandin E1 decreased adhesion between vascular endothelial cells and monocytes and suppressed TNF-induced NF-kappaB activation and reactive oxygen species production.