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

Journal of Inflammation

Lynnette R Ferguson¹  Richard F Mithen²  Gareth Marlow¹  Danielle L Folkard² 

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

关键词: Crohn’s disease;    Inflammation;    NOD2;    Sulforaphane;   

Others  :  1137205
DOI  :  10.1186/s12950-015-0051-x

 received in 2014-05-16, accepted in 2015-01-08,  发布年份 2015

【 摘 要 】

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.

【 授权许可】

   
2015 Folkard et al.; licensee BioMed Central.

【 图 表 】

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