PT  - JOURNAL ARTICLE
AU  - Andrew Durham
AU  - Elen Jazrawi
AU  - Jo Ann Rhodes
AU  - Cara Williams
AU  - Ian Kilty
AU  - Peter Barnes
AU  - K. Fan Chung
AU  - Ian Adcock
TI  - The anti-inflammatory effects of sulforaphane are not mediated by the Nrf2 pathway
DP  - 2014 Sep 01
TA  - European Respiratory Journal
PG  - P3332
VI  - 44
IP  - Suppl 58
4099  - http://erj.ersjournals.com/content/44/Suppl_58/P3332.short
4100  - http://erj.ersjournals.com/content/44/Suppl_58/P3332.full
SO  - Eur Respir J2014 Sep 01; 44
AB  - Sulforaphane (SFN) is a naturally occurring compound, found in cruciferous vegetables. SFN is a potent activator of the endogenous anti-oxidant transcription factor nuclear factor (erythroid-derived 2)-like 2 (Nrf2). Due to its anti-oxidant and anti-inflammatory properties SFN has been identified as a potential treatment for a number of diseases including chronic obstructive pulmonary (COPD). We confirmed that SFN activates of the Nrf2 pathway and induces the expression of haemoxygenase (HO)-1 and NAD(P)H:Quinone Oxireductase (NQO)-1. SFN suppressed interleukin (IL)-1b-induced and IL-1b plus oxidative stress (hydrogen peroxide, H2O2)-induced CXCL8 expression in a concentration-dependent manner in human bronchial epithelial and monocyte cell lines. Nrf2 siRNA significantly reduced the ability of SFN to enhance Nrf2-mediated induction of HO-1 and NQO-1 without any effect on the ability of SFN to suppress IL-1b- and IL-1b+H2O2-induced CXCL8 expression in these cells. Our results suggest that the anti-inflammatory effects of SFN occur independently of Nrf2 in human airway epithelial cells and macrophages.Figure legend. Nrf2 knockdown using siRNA abrogates the ability of sulpforophane to induce Nrf2 activation (A & B) and that of the downstream target NQO-1 (c & d) in BEAS-2B cells. Nrf2 knockdown does not have a significant effect on the ability of sulforophane to suppress IL-1b-induced CXCL8 release in BEAS-2B or U937 cells (e & f).