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Effect of Sinigrin on Vascular Cell Adhesion Molecule‐1 Expression in TNF‐α‐Stimulated Mouse Vascular Smooth Muscle Cells via Downregulation of NF‐κB Signaling Pathways
Author(s) -
Lee Hee Weon,
Lee Kyoung Ran
Publication year - 2015
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.29.1_supplement.593.15
Subject(s) - sinigrin , cell adhesion molecule , vascular smooth muscle , cell adhesion , nf κb , microbiology and biotechnology , chemistry , inflammation , downregulation and upregulation , western blot , signal transduction , tumor necrosis factor alpha , vcam 1 , cell , biochemistry , biology , immunology , endocrinology , smooth muscle , glucosinolate , gene , agronomy , brassica
Atherosclerosis is a chronic inflammatory disorder of the arteries. Since chronic inflammation increases the expression of various adhesion molecules, interfering with the expression of the adhesion molecules could be an important therapeutic target of inflammatory disorders. Sinigrin has been known to have a variety of biological activities including anti‐inflammatory activities. However, other biological activities of sinigrin and its molecular mechanisms have not been known and characterized in detail yet. In the present study, we examined the effect of sinigrin on the expression of the vascular cell adhesion molecule‐1 (VCAM‐1) in TNF‐α‐induced vascular smooth muscle cells (VSMCs). Western blot analysis and ELISA showed that the increased expression of VCAM‐1 by TNF‐α was significantly suppressed by the pre‐treatment of sinigrin (1‐100 μg/ml) for 2 hours. Our data also revealed that sinigrin inhibited the nuclear translocation of NF‐κB induced by TNF‐α. Overall, these results suggest that sinigrin inhibits TNF‐α‐stimulated VCAM‐1 expression through the suppression of NF‐κB signaling pathways. Therefore, sinigrin is considered as a therapeutic agent to reduce the risk of atherosclerosis.