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An ethanol extract Gastrodia elata inhibits TNF‐α‐induced cell adhesion in human umbilical vein endothelial cells
Author(s) -
Hwang Sun Mi,
Kang Dae Gill,
Lee Yun Jung,
Kim Jin Sook,
Lee Ho Sub
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1128.19
Subject(s) - umbilical vein , cell adhesion molecule , e selectin , cell adhesion , tumor necrosis factor alpha , human umbilical vein endothelial cell , chemistry , vcam 1 , endothelial activation , endothelial stem cell , gastrodia elata , cytokine , intracellular , monocyte , soluble cell adhesion molecules , inflammation , microbiology and biotechnology , immunology , icam 1 , biochemistry , cell , biology , medicine , in vitro , pathology , alternative medicine , traditional chinese medicine
Gastrodia elata is Oriental herbs that have been widely used for the treatment of inflammatory diseases. Endothelial dysfunction and associated vascular inflammatory processes play pivotal roles in the development of atherosclerosis. The present study was designed to examine the effect of ethanol extract of Gastrodia elata (EGE) on vascular inflammation response in primary cultured human umbilical vein endothelial cells (HUVEC). EGE significantly inhibited tumor necrosis factor‐α (TNF‐α)‐induced increase in monocyte adhesion to HUVEC in dose‐dependent manner. In addition, pretreatment with EGE attenuated the expression levels of cell adhesion molecules such as intercellular cell adhesion molecule‐1 (ICAM‐1), vascular cell adhesion molecule‐1 (VCAM‐1), and endothelial selectin (E‐selectin) induced by TNF‐α in HUVEC. Real time RT‐PCR also showed that EGE decreased the expression levels of ICAM‐1, VCAM‐1, E‐selectin, MCP‐1, and IL‐8 mRNA. Furthermore, EGE significantly inhibited the TNF‐α‐induced intracellular reactive oxygen species (ROS) production and NF‐κB activation by preventing IκB phophorylation. In conclusion, EGE has an anti‐inflammatory activity, which is at least in part the result of it reducing the cytokine‐induced HUVEC adhesion to monocytes through the inhibition of intracellular ROS production, NF‐κB activation, and cell adhesion molecules expression in HUVEC.