Resveratrol suppresses tumor necrosis factor-α-induced fractalkine expression in endothelial cells

被引：55

作者：

Moon, Sang-Ok

Kim, Won

Sung, Mi Jeong

Lee, Sik

Kang, Kyung Pyo

Kim, Duk Hoon

Lee, Sang Yong

So, June-No

Park, Sung Kwang

机构：

[1] Chonbuk Natl Univ, Renal Reg Lab, Sch Med, Jeonju 561180, South Korea

[2] Chonbuk Natl Univ, Dept Diagnost Radiol, Sch Med, Jeonju 561180, South Korea

[3] Chonbuk Natl Univ, Res Inst Clin Med, Sch Med, Jeonju 561180, South Korea

[4] Woosuk Univ, Dept Pharmaceut Engn, Jeonju 561180, South Korea

来源：

MOLECULAR PHARMACOLOGY | 2006年 / 70卷 / 01期

关键词：

D O I：

10.1124/mol.106.022392

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

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)-alpha. TNF-alpha significantly induced fractalkine mRNA and protein expression in endothelial cells. Resveratrol strongly suppressed TNF-alpha-induced fractalkine expression in endothelial cells through suppression of nuclear factor-kappa B and Sp1 activities. Resveratrol decreased the number of TNF-alpha-induced fractalkine-positive endothelial cells and CX3CR1-positive cells determined by flow cytometric analysis. Resveratrol suppressed TNF-alpha-stimulated monocytes adhesion to human umbilical vein endothelial cells. Immunohistochemical analysis revealed that resveratrol suppressed TNF-alpha-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.

引用

页码：112 / 119

页数：8

共 41 条

[1] Tumor necrosis factor-α induces fractalkine expression preferentially in arterial endothelial cells and mithramycin A suppresses TNF-α-induced fractalkine expression [J].