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Effect of Zanthoxylum schinifolium on TNF‐α‐induced vascular inflammation in human umbilical vein endothelial cells
Author(s) -
Cao Li Hua,
Lee Yun Jung,
Kang Dae Gill,
Moon Mi Kyoung,
Hwang Sun Mi,
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.1128.16
Subject(s) - umbilical vein , cell adhesion molecule , cell adhesion , inflammation , microbiology and biotechnology , tumor necrosis factor alpha , reactive oxygen species , adhesion , biology , chemistry , biochemistry , cell , immunology , in vitro , organic chemistry
Pro‐inflammatory cytokines induced the injury of endothelial cells caused by increases of adhesion molecules, leading to vascular inflammation and the development of atherosclerosis. In this study, we investigated whether an ethanol extract of Zanthoxylum schinifolium (EZS) inhibited the expression level of cellular adhesion molecules in human umbilical vein endothelial cells (HUVEC). EZS suppressed the cell adhesions between HUVECs and HL‐60 cells induced by TNF‐α in a dose dependent manner. EZS also suppressed the expression levels of adhesion molecules such as intracellular cell adhesion molecule‐1 (ICAM‐1) and vascular cell adhesion molecule‐1 (VCAM‐1) induced by TNF‐α. TNF‐α‐induced increases of MCP‐1 and IL‐8 mRNA expression were also attenuated by pretreatment with EZS. In addition, treatment of HUVEC with EZS suppressed TNF‐α‐induced reactive oxygen species (ROS) production. Furthermore, EZS inhibited NF‐κB activation and IκB‐αphosphorylation induced by TNF‐α, subsequent degradation of IκB‐α. These results demonstrated that EZS could suppress vascular inflammatory process, which may be closely related with the inhibition of ROS and NF‐κB activation in HUVEC.