PT  - JOURNAL ARTICLE
AU  - Sang-Ok Moon
AU  - Won Kim
AU  - Mi Jeong Sung
AU  - Sik Lee
AU  - Kyung Pyo Kang
AU  - Duk Hoon Kim
AU  - Sang Yong Lee
AU  - June-No So
AU  - Sung Kwang Park
TI  - Resveratrol Suppresses Tumor Necrosis Factor-α-Induced Fractalkine Expression in Endothelial Cells
AID  - 10.1124/mol.106.022392
DP  - 2006 Jul 01
TA  - Molecular Pharmacology
PG  - 112--119
VI  - 70
IP  - 1
4099  - http://molpharm.aspetjournals.org/content/70/1/112.short
4100  - http://molpharm.aspetjournals.org/content/70/1/112.full
SO  - Mol Pharmacol2006 Jul 01; 70
AB  - Up-regulation of fractalkine is involved in vascular and tissue damage in inflammatory conditions. Resveratrol has been shown to have anti-inflammatory, antioxidant, and antitumor activities. Its regulatory effects on expression of fractalkine in vascular endothelial cells and fractalkine receptor CX3CR1 in monocytes have not been studied. We evaluated the effects of resveratrol on fractalkine expression in human umbilical vein endothelial cells and CX3CR1 expression in THP-1 cells in response to treatment with tumor necrosis factor (TNF)-α. TNF-α significantly induced fractalkine mRNA and protein expression in endothelial cells. Resveratrol strongly suppressed TNF-α-induced fractalkine expression in endothelial cells through suppression of nuclear factor-κB and Sp1 activities. Resveratrol decreased the number of TNF-α-induced fractalkine-positive endothelial cells and CX3CR1-positive cells determined by flow cytometric analysis. Resveratrol suppressed TNF-α-stimulated monocytes adhesion to human umbilical vein endothelial cells. Immunohistochemical analysis revealed that resveratrol suppressed TNF-α-induced arterial endothelial fractalkine expression in heart, kidney, and intestine and decreased ED-1-positive cell infiltration in intestinal villi. Resveratrol may provide a new pharmacological approach for suppressing fractalkine/CX3CR1-mediated injury in inflammatory conditions.