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Effect of Lycopus lucidus on high glucose‐induced vascular inflammation in human umbilical vein endothelial cells
Author(s) -
Lee Yun Jung,
Kang Dae Gill,
Moon Mi Kyoung,
Cao Li Hua,
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.1128.15
Subject(s) - umbilical vein , reactive oxygen species , inflammation , pharmacology , chemistry , proinflammatory cytokine , western blot , tumor necrosis factor alpha , cell adhesion molecule , monocyte , endothelial stem cell , biology , biochemistry , immunology , in vitro , gene
High glucose‐induced vascular inflammatory process has been suggested to play a key role in the initiation and progression of atherosclerosis. Lycopus lucidus Turcz. has been used as an Oriental traditional medicine and its crude drug is known to have an anti‐inflammatory effect. Thus we investigated whether the aqueous extract of the leaves of L. lucidus Turcz . (ALT) suppresses vascular inflammatory process induced by high glucose in primary cultured human umbilical vein endothelial cells (HUVEC). Western blot analysis revealed that incubation of HUVEC with high glucose increased cell adhesion molecules (CAMs) expression levels, which were significantly attenuated by pretreatment with ALT in a dose‐dependent manner. The enhanced cell adhesion between monocyte and HUVEC induced by high glucose was also blocked by pretreatment with ALT. High glucose induced hydrogen peroxide production and DCF‐sensitive intracellular reactive oxygen species (ROS) formation were also inhibited by pretreatment with ALT. In addition, ALT suppressed the translocation and promoter transcriptional activity of NF‐κB increased in high glucose condition. Taken together, the present data suggested that ALT could suppress high glucose‐induced vascular inflammatory process, which may be closely related with the inhibition of ROS and NF‐κB activation in HUVEC.

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