Anti-TNF-α Activity of Portulaca oleracea in Vascular Endothelial Cells

Vascular inflammation plays a key role in the pathogenesis and progression of atherosclerosis, a main complication of diabetes. The present study investigated whether an aqueous extract of Portulaca oleracea (AP) prevents the TNF-alpha-induced vascular inflammatory process in the human umbilical vein endothelial cell (HUVEC). The stimulation of TNF-alpha induced overexpression of adhesion molecules affects vascular cell adhesion molecule (VCAM)-1, intercellular adhesion molecule (ICAM)-1 and E-selectin for example. However, AP significantly suppressed TNF-alpha-induced over-expression of these adhesion molecules in a dose-dependent manner. In addition, pretreatment with AP dose-dependently reduced an increase of the adhesion of HL-60 cells to TNF-alpha-induced HUVEC. Furthermore, we observed that stimulation of TNF-alpha significantly increased intracellular reactive oxygen species (ROS) production. However, pretreatment with AP markedly blocked TNF-alpha-induced ROS production in a dose-dependent manner. The western blot and immunofluorescence analysis showed that AP inhibited the translocation of p65 NF-kappa B to the nucleus. In addition, AP suppressed the TNF-alpha-induced degradation of I kappa B-alpha and attenuated the TNF-alpha-induced NF-kappa B binding. AP also effectively reduced TNF-alpha-induced mRNA expressions of monocyte chemoattractant protein (MCP)-1 and interleukin (IL)-8 in a dose-dependent manner. Taken together, AP prevents the vascular inflammatory process through the inhibition of intracellular ROS production and NF-kappa B activation as well as the reduction of adhesion molecule expression in TNF-alpha-induced HUVEC. These results suggested that AP might have a potential therapeutic effect by inhibiting the vascular inflammation process in vascular diseases such as atherosclerosis.