Sulforaphane suppresses lipopolysaccharide-induced cyclooxygenase-2 (COX-2) expression through the modulation of multiple targets in COX-2 gene promoter

Int Immunopharmacol. 2007 Dec 15;7(13):1776-83. doi: 10.1016/j.intimp.2007.09.018. Epub 2007 Oct 5.

Abstract

Sulforaphane is a natural, biologically active compound extracted from cruciferous vegetables such as broccoli and cabbage. It possesses potent anti-inflammation and anti-cancer properties. The mechanism by which sulforaphane suppresses COX-2 expression remains poorly understood. In the present report, we investigated the effect of sulforaphane on the expression of COX-2 in lipopolysaccharide (LPS)-activated Raw 264.7 cells. Sulforaphane significantly suppressed the LPS-induced COX-2 protein and mRNA expression in a dose-dependent manner. The ability of sulforaphane to suppress the expression of the COX-2 was investigated using luciferase reporters controlled by various cis-elements in COX-2 promoter region. Electrophoretic mobility shift assay (EMSA) verified that NF-kappaB, C/EBP, CREB and AP-1 were identified as responsible for the sulforaphane-mediated COX-2 down-regulation. In addition, we demonstrated the signal transduction pathway of mitogen-activated protein kinase (MAP kinase) in LPS-induced COX-2 expression. Taken together, these results demonstrate that sulforaphane effectively suppressed the LPS-induced COX-2 protein via modulation of multiple core promoter elements (NF-kappaB, C/EBP, CREB and AP-1) in the COX-2 transcriptional regulation. These results will provide new insights into the anti-inflammatory and anti-carcinogenic properties of sulforaphane.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • CCAAT-Enhancer-Binding Proteins / antagonists & inhibitors
  • CCAAT-Enhancer-Binding Proteins / metabolism
  • Cell Line
  • Cyclic AMP Response Element-Binding Protein / antagonists & inhibitors
  • Cyclic AMP Response Element-Binding Protein / metabolism
  • Cyclooxygenase 2 / genetics*
  • Cyclooxygenase 2 Inhibitors / pharmacology*
  • Isothiocyanates
  • Lipopolysaccharides / pharmacology*
  • Macrophages / enzymology
  • Mice
  • Mitogen-Activated Protein Kinases / metabolism
  • NF-kappa B / antagonists & inhibitors
  • Phosphorylation
  • Promoter Regions, Genetic*
  • Sulfoxides
  • Thiocyanates / pharmacology*

Substances

  • CCAAT-Enhancer-Binding Proteins
  • Cyclic AMP Response Element-Binding Protein
  • Cyclooxygenase 2 Inhibitors
  • Isothiocyanates
  • Lipopolysaccharides
  • NF-kappa B
  • Sulfoxides
  • Thiocyanates
  • Ptgs2 protein, mouse
  • Cyclooxygenase 2
  • Mitogen-Activated Protein Kinases
  • sulforaphane