Estrogen receptor-independent inhibition of tumor necrosis factor-α gene expression by phytoestrogen equol is mediated by blocking nuclear factor-κB activation in mouse macrophages

Jong Soon Kang, Yeo Dae Yoon, Mi Hwa Han, Sang Bae Han, Kiho Lee, Moo Rim Kang, Eun Yi Moon, Young Jin Jeon, Song Kyu Park, Hwan Mook Kim

Research output: Contribution to journalArticlepeer-review

29 Scopus citations

Abstract

Equol has been suggested to possess protective effects on bone. However, the underlying mechanism of osteoprotective effect of equol has not been fully understood. In the present study, we examined the effect of equol on tumor necrosis factor-α (TNF-α) gene expression to elucidate a possible mechanism by which equol exerts osteoprotective effect. In vivo administration of equol inhibited TNF-α production by peritoneal macrophages isolated from LPS-treated mice. Equol also dose-dependently inhibited TNF-α production and TNF-α mRNA expression in LPS-stimulated mouse macrophages. Pretreatment of cells with ICI 182.780, an estrogen receptor antagonist, had no effect on the inhibitory efficacy of equol on LPS-induced TNF-α production. Further study demonstrated that equol inhibited NF-κB DNA binding and NF-κB-dependent reporter gene expression in activated RAW 264.7 cells. Moreover, equol blocked degradation of IκBα and IκBβ and nuclear translocation of p65 subunit of NF-κB in activated RAW 264.7 cells. These results suggest that the inhibitory effect of equol on TNF-α expression is mediated, at least in part, by blocking NF-κB activation and the inhibition of TNF-α expression by equol might be involved in its osteoprotective effect.

Original languageEnglish (US)
Pages (from-to)136-143
Number of pages8
JournalBiochemical Pharmacology
Volume71
Issue number1-2
DOIs
StatePublished - Dec 19 2005

Bibliographical note

Funding Information:
This research was supported by a grant from KRIBB Research Initiative Program.

Copyright:
Copyright 2008 Elsevier B.V., All rights reserved.

Keywords

  • Equol
  • Osteoporosis
  • TNF-α ;NF-κB

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