Sulforaphane Inhibits TNF-α-Induced Adhesion Molecule Expression Through the Rho A/ROCK/NF-κB Signaling Pathway

Endothelial dysfunction is an early indicator of cardiovascular diseases. Increased stimulation of tumor necrosis factor-alpha (TNF-alpha) triggers the inflammatory mediator secretion of endothelial cells, leading to atherosclerotic risk. In this study, we investigated whether sulforaphane (SFN) affected the expression of intracellular adhesion molecule-1 (ICAM-1) in TNF-alpha-induced ECV 304 endothelial cells. Our data showed that SFN attenuated TNF-alpha-induced expression of ICAM-1 in ECV 304 cells. Pretreatment of ECV 304 cells with SFN inhibited dose-dependently the secretion of proinflammatory cytokines, such as interleukin (IL)-1 beta, IL-6, and IL-8. SFN inhibited TNF-alpha-induced nuclear factor-kappa B (NF-kappa B) DNA binding activity. Furthermore, SFN decreased TNF-alpha-mediated phosphorylation of I kappa B kinase (IKK) and I kappa B alpha, Rho A, ROCK, ERK1/2, and plasminogen activator inhibitor-1 (PAI-1) levels. Collectively, SFN inhibited the NF-kappa B DNA binding activity and downregulated the TNF-alpha-mediated induction of ICAM-1 in endothelial cells by inhibiting the Rho A/ROCK/NF-kappa B signaling pathway, suggesting the beneficial effects of SFN on suppression of inflammation within the atherosclerotic lesion.