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Sulforaphane inhibition of monocyte adhesion via the suppression of ICAM-1 and NF-κB is dependent upon glutathione depletion in endothelial cells

2008; Elsevier BV; Volume: 48; Issue: 1 Linguagem: Inglês

10.1016/j.vph.2007.11.006

1879-3649

Yen‐Chin Liu, Chia‐Wen Hsieh, Yu‐Chun Weng, Shu-Hui Chuang, Cheng-Yuan Hsieh, Being‐Sun Wung,

IL-33, ST2, and ILC Pathways

Sulforaphane (SFN) is an isothiocyanate found in cruciferous vegetables. We here report that SFN is a potent inhibitor of LPS-induced monocyte adhesion, and also blocks the gene expression of the adhesion molecule, ICAM-1, at non-toxic concentrations. Downstream of ICAM-1, NF- kappaB activity was also found to be abolished in a dose-and time-dependent by SFN in LPS-treated endothelial cells (ECs). SFN exerts its suppressive effects on NF- kappaB activity in these cells by preventing the degradation of IkappaB-alpha. Interestingly, the inhibition of P65 translocation and IkappaB-alpha degradation was reversed slightly after 12 hours pretreatment. The intracellular GSH levels in SFN-treated ECs were observed to be reduced, the time course coincident with the suppression of P65 translocation and IkappaB-alpha degradation. NAC and GSH reverse the inhibitory effects of SFN upon p65 translocation and IkappaB-alpha degradation when preincubated with this agent. Furthermore, the use of BSO to decrease intracellular GSH levels further enhanced the effects of SFN. These data thus suggest that the anti-inflammatory mechanisms of SFN are dependent upon intracellular glutathione level.