Sulforaphane Inhibits TNF

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

Inflamm Res. 2009 Aug;58(8):513-21. Epub 2009 Mar 11.

Chen XL, Dodd G, Kunsch C.

Discovery Research, AtheroGenics, Inc., 8995 Westside Parkway, Alpharetta, GA 30004, USA.

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.



Note from ISS:  Several crucifer sprouts including broccoli sprouts are currently the most potent natural source of sulforaphane known.  They often produce 10 to 100 times the amount of sulforaphane as their corresponding mature vegetables. (“Broccoli sprouts: an exceptionally rich source of inducers of enzymes that protect against chemical carcinogens.”, Proc Natl Acad Sci U S A 1997 Sep 16;94(19):10367-72.)