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Inflamm Res. 2009 Aug;58(8):513-21. doi: 10.1007/s00011-009-0017-7. Epub 2009 Mar 11.

Sulforaphane inhibits TNF-alpha-induced activation of p38 MAP kinase and VCAM-1 and MCP-1 expression in endothelial cells.

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  • 1Discovery Research, AtheroGenics, Inc., 8995 Westside Parkway, Alpharetta, GA 30004, USA. xchen@atherogenics.com

Abstract

OBJECTIVE AND DESIGN:

To investigate the effects of sulforaphane on endothelial inflammatory gene expression in endothelial cells.

MATERIALS AND METHODS:

Human aortic endothelial cells were used in the study.

RESULTS:

One-hour pretreatment of endothelial cells (EC) with sulforaphane (1-4 muM) 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-kappaB nuclear binding activity, IkappaB-alpha degradation or activation of NF-kappaB-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.

CONCLUSION:

These data suggest that sulforaphane may be useful as a therapeutic agent for the treatment of inflammatory diseases.

[PubMed - indexed for MEDLINE]
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