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Effect of Paeotang on TNF‐α‐induced vascular inflammation in human umbilical vein endothelial cells (1158.4)
Author(s) -
Kim Dae Hwan,
Lee Yun Jung,
Yoon Jung Joo,
Lee So Min,
Kang Dae Gill,
Lee Ho Sub
Publication year - 2014
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.28.1_supplement.1158.4
Subject(s) - umbilical vein , inflammation , tumor necrosis factor alpha , cell adhesion molecule , western blot , human umbilical vein endothelial cell , cell adhesion , intercellular adhesion molecule 1 , intracellular , matrix metalloproteinase , chemistry , endothelial stem cell , microbiology and biotechnology , immunology , biology , cell , in vitro , biochemistry , gene
Vascular inflammation is an important event in the development of vascular disease such as tumor progression and atherosclerosis. Paeotang, a formula composed of eight herbs, has been used for extravasated blood in Korean medicine. In this study, the inhibitory effects of Paeotang on TNF‐α‐induced vascular inflammation process in human umbilical vein endothelial cells (HUVEC). Pretreatment with Paeotang decreased TNF‐α‐induced adhesion HL‐60 monocytic cells, as well as mRNA and protein expression of intracellular adhesion molecule‐1 (ICAM‐1), vascular cell adhesion molecule‐1 (VCAM‐1), and endothelial cell selectin (E‐selectin). Paeotang also dose‐dependently inhibited TNF‐α‐induced matrix metalloproteinase‐2 and ‐9 expression. Furthermore, Paeotang significantly decreased TNF‐α‐induced intracellular reactive oxygen species (ROS) production. The western blot and immunofluorescence analysis showed that Paeotang suppressed the translocation of p65 NF‐κB to the nucleus. In addition Paeotang inhibited the TNF‐α‐induced degradation of IκB‐α, and inhibitor of NF‐κB, by inhibiting the phosphorylation of IκB‐α. These results suggest that Paeotang may be a therapetic agent in vascular inflammation through inhibition of ROS/NF‐κB pathway.