title: Sulforaphane inhibits TNF-α-induced adhesion molecule expression through the Rho A/ROCK/NF-κB signaling pathway.
abstract: Endothelial dysfunction is an early indicator of cardiovascular diseases. Increased stimulation of tumor necrosis factor-α (TNF-α) 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-α-induced ECV 304 endothelial cells. Our data showed that SFN attenuated TNF-α-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)-1β, IL-6, and IL-8. SFN inhibited TNF-α-induced nuclear factor-κB (NF-κB) DNA binding activity. Furthermore, SFN decreased TNF-α-mediated phosphorylation of IκB kinase (IKK) and IκBα, Rho A, ROCK, ERK1/2, and plasminogen activator inhibitor-1 (PAI-1) levels. Collectively, SFN inhibited the NF-κB DNA binding activity and downregulated the TNF-α-mediated induction of ICAM-1 in endothelial cells by inhibiting the Rho A/ROCK/NF-κB signaling pathway, suggesting the beneficial effects of SFN on suppression of inflammation within the atherosclerotic lesion.
authors.affiliation: 1 Department of Holistic Wellness, Ming Dao University , ChangHua, Taiwan .
authors.forename: Chi-Nan
authors.initials: CN
authors.lastname: Hung
authors.forename: Hui-Pei
authors.initials: HP
authors.lastname: Huang
authors.forename: Chau-Jong
authors.initials: CJ
authors.lastname: Wang
authors.forename: Kai-Li
authors.initials: KL
authors.lastname: Liu
authors.forename: Chong-Kuei
authors.initials: CK
authors.lastname: Lii
mesh_terms: D002460:Cell Line; D015536:Down-Regulation / Q000187:drug effects; D042783:Endothelial Cells / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics* / Q000378:metabolism; D017879:Isothiocyanates / Q000494:pharmacology*; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects*; D013454:Sulfoxides; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism*; D054460:rho-Associated Kinases / Q000235:genetics / Q000378:metabolism*; D020742:rhoA GTP-Binding Protein / Q000235:genetics / Q000378:metabolism*
chemical_list: D017879:Isothiocyanates; D016328:NF-kappa B; D013454:Sulfoxides; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D054460:rho-Associated Kinases; D020742:rhoA GTP-Binding Protein; C016766:sulforaphane
keywords: Rho A; atherosclerosis; proinflammation; sulforaphane; tumor necrosis factor-α