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Gardenia jasminoides inhibits tumor necrosis factor‐alpha‐induced vascular inflammation in endothelial cells
Author(s) -
Hwang Sun Mi,
Lee Yun Jung,
Yoon Jung Joo,
Lee So Min,
Kang Dae Gill,
Lee Ho Sub
Publication year - 2010
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.3099
Subject(s) - tumor necrosis factor alpha , e selectin , cell adhesion molecule , gardenia jasminoides , umbilical vein , inflammation , endothelium , cell adhesion , endothelial stem cell , medicine , vcam 1 , soluble cell adhesion molecules , monocyte , immunology , cancer research , chemistry , endocrinology , icam 1 , cell , pathology , biochemistry , in vitro , alternative medicine
Abstract Inflammatory mediators such as tumor necrosis factor‐alpha (TNF‐α) 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‐α‐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‐α‐induced nuclear p65 nuclear factor‐kappa B (NF‐κB) translocation, suggesting that EGJ primarily affects the TNF‐α‐induced NF‐κB signaling pathway. Taken together, we provided here the first evidence showing that EGJ is able to inhibit TNF‐α‐induced NF‐κB 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. Copyright © 2010 John Wiley & Sons, Ltd.