Xi-Lin Chen1, Geraldine Dodd, Charles Kunsch. 1. Discovery Research, AtheroGenics, Inc., 8995 Westside Parkway, Alpharetta, GA 30004, USA. xchen@atherogenics.com
Abstract
OBJECTIVE AND DESIGN: To investigate the effects of sulforaphane on endothelial inflammatory gene expression in endothelial cells. MATERIALS AND METHODS: Human aortic endothelial cells were used in the study. RESULTS: One-hour pretreatment of endothelial cells (EC) with sulforaphane (1-4 muM) suppressed TNF-alpha-induced MCP-1 and VCAM-1 mRNA and protein levels, but had no effect on TNF-alpha-induced ICAM-1 expression. Sulforaphane also inhibited TNF-alpha-induced activation of p38 MAP kinase, but not c-Jun-N-terminal kinase. Sulforaphane had no effect on TNF-alpha-induced NF-kappaB nuclear binding activity, IkappaB-alpha degradation or activation of NF-kappaB-driven transcriptional activity. Expression of dominant negative Nrf2 inhibited sulforaphane-induced antioxidant response element (ARE)-driven promoter activity, but had no effect on sulforaphane-mediated inhibition of VCAM-1 and MCP-1 expression. CONCLUSION: These data suggest that sulforaphane may be useful as a therapeutic agent for the treatment of inflammatory diseases.
OBJECTIVE AND DESIGN: To investigate the effects of sulforaphane on endothelial inflammatory gene expression in endothelial cells. MATERIALS AND METHODS:Human aortic endothelial cells were used in the study. RESULTS: One-hour pretreatment of endothelial cells (EC) with sulforaphane (1-4 muM) suppressed TNF-alpha-induced MCP-1 and VCAM-1 mRNA and protein levels, but had no effect on TNF-alpha-induced ICAM-1 expression. Sulforaphane also inhibited TNF-alpha-induced activation of p38 MAP kinase, but not c-Jun-N-terminal kinase. Sulforaphane had no effect on TNF-alpha-induced NF-kappaB nuclear binding activity, IkappaB-alpha degradation or activation of NF-kappaB-driven transcriptional activity. Expression of dominant negative Nrf2 inhibited sulforaphane-induced antioxidant response element (ARE)-driven promoter activity, but had no effect on sulforaphane-mediated inhibition of VCAM-1 and MCP-1 expression. CONCLUSION: These data suggest that sulforaphane may be useful as a therapeutic agent for the treatment of inflammatory diseases.
Authors: K Itoh; T Chiba; S Takahashi; T Ishii; K Igarashi; Y Katoh; T Oyake; N Hayashi; K Satoh; I Hatayama; M Yamamoto; Y Nabeshima Journal: Biochem Biophys Res Commun Date: 1997-07-18 Impact factor: 3.575
Authors: Robert D Bongard; Gary S Krenz; Adam J Gastonguay; Carol L Williams; Brian J Lindemer; Marilyn P Merker Journal: Free Radic Biol Med Date: 2011-01-14 Impact factor: 7.376
Authors: Kaustabh Ghosh; Mathumai Kanapathipillai; Netanel Korin; Jason R McCarthy; Donald E Ingber Journal: Nano Lett Date: 2011-12-28 Impact factor: 11.189
Authors: Noha M Shawky; Prahalathan Pichavaram; George S G Shehatou; Ghada M Suddek; Nariman M Gameil; John Y Jun; Lakshman Segar Journal: J Nutr Biochem Date: 2016-03-10 Impact factor: 6.048
Authors: Paul M Holloway; Scarlett Gillespie; Felix Becker; Shantel A Vital; Victoria Nguyen; J Steven Alexander; Paul C Evans; Felicity N E Gavins Journal: Vascul Pharmacol Date: 2016-07-08 Impact factor: 5.773