Gardenia jasminoides inhibits tumor necrosis factor-alpha-induced vascular inflammation in endothelial cells.

Inflammatory mediators such as tumor necrosis factor-alpha (TNF-alpha) enhance binding of low-density lipoprotein to endothelium and upregulate the expression of endothelial leukocyte adhesion molecules during atherogenesis. The present study examined the effect of ethanol extract of Gardenia jasminoides (EGJ) on vascular inflammation in primary cultured human umbilical vein endothelial cells (HUVEC). TNF-alpha-induced the expression of vascular cell adhesion molecule-1 (VCAM-1) and endothelial cell-selectin (E-selectin) expression was inhibited in HUVEC pretreated with EGJ. In a functional study, EGJ dose-dependently attenuated adhesion of HL-60 monocytes to endothelial monolayers. A further analysis indicated that EGJ attenuated TNF-alpha-induced nuclear p65 nuclear factor-kappa B (NF-kappaB) translocation, suggesting that EGJ primarily affects the TNF-alpha-induced NF-kappaB signaling pathway. Taken together, we provided here the first evidence showing that EGJ is able to inhibit TNF-alpha-induced NF-kappaB activation, adhesion molecule expression, and monocyte-endothelial interaction, suggesting an anti-inflammatory role of EGJ, which may be useful in preventing vascular diseases, such as atherosclerosis.