Journal
INFLAMMATION RESEARCH
Volume 58, Issue 8, Pages 513-521Publisher
SPRINGER BASEL AG
DOI: 10.1007/s00011-009-0017-7
Keywords
Sulforaphane; Monocyte chemoattractant protein-1; Vascular cell adhesion molecule-1; TNF-alpha; p38 MAP kinase; Nrf2; Endothelial cells
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To investigate the effects of sulforaphane on endothelial inflammatory gene expression in endothelial cells. Human aortic endothelial cells were used in the study. One-hour pretreatment of endothelial cells (EC) with sulforaphane (1-4 mu M) suppressed TNF-alpha-induced MCP-1 and VCAM-1 mRNA and protein levels, but had no effect on TNF-alpha-induced ICAM-1 expression. Sulforaphane also inhibited TNF-alpha-induced activation of p38 MAP kinase, but not c-Jun-N-terminal kinase. Sulforaphane had no effect on TNF-alpha-induced NF-kappa B nuclear binding activity, I kappa B-alpha degradation or activation of NF-kappa B-driven transcriptional activity. Expression of dominant negative Nrf2 inhibited sulforaphane-induced antioxidant response element (ARE)-driven promoter activity, but had no effect on sulforaphane-mediated inhibition of VCAM-1 and MCP-1 expression. These data suggest that sulforaphane may be useful as a therapeutic agent for the treatment of inflammatory diseases.
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