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J Inflamm (Lond). 2015 Jan 20;12:6. doi: 10.1186/s12950-015-0051-x. eCollection 2015.

Effect of Sulforaphane on NOD2 via NF-κB: implications for Crohn's disease.

Author information

1
Food and Health Programme, Institute of Food Research, Norwich Research Park, Norwich, UK.
2
Nutrigenomics New Zealand, University of Auckland, Private Bag 92019, Auckland, 1142 New Zealand.

Abstract

BACKGROUND:

Sulforaphane has well established anti-cancer properties and more recently anti-inflammatory properties have also been determined. Sulforaphane has been shown to inhibit PRR-mediated pro-inflammatory signalling by either directly targeting the receptor or their downstream signalling molecules such as the transcription factor, NF-κB. These results raise the possibility that PRR-mediated inflammation could be suppressed by specific dietary bioactives. We examined whether sulforaphane could suppress NF-κB via the NOD2 pathway.

METHODS:

Human embryonic kidney 293T (HEK293T) cells were stably transfected with NOD2 variants and the NF-κB reporter, pNifty2-SEAP. The cells were co-treated with sulforaphane and MDP and secreted alkaline phosphatase (SEAP) production was determined.

RESULTS:

We found that sulforaphane was able to significantly suppress the ligand-induced NF-κB activity at physiologically relevant concentrations, achievable via the consumption of broccoli within the diet.

CONCLUSIONS:

These results demonstrate that the anti-inflammatory role of sulforaphane is not restricted to LPS-induced inflammatory signalling. These data add to the growing evidence that PRR activation can be inhibited by specific phytochemicals and thus suggests that diet could be a way of controlling inflammation. This is particularly important for a disease like Crohn's disease where diet can play a key role in relieving or exacerbating symptoms.

KEYWORDS:

Crohn’s disease; Inflammation; NOD2; Sulforaphane

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