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Molecular Pharmacology

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Research ArticleArticle

Glabridin Suppresses Intercellular Adhesion Molecule-1 Expression in Tumor Necrosis Factor-α-Stimulated Human Umbilical Vein Endothelial Cells by Blocking Sphingosine Kinase Pathway: Implications of Akt, Extracellular Signal-Regulated Kinase, and Nuclear Factor-κB/Rel Signaling Pathways

Jong Soon Kang, Yeo Dae Yoon, Mi Hwa Han, Sang-Bae Han, Kiho Lee, Ki Hoon Lee, Song-Kyu Park and Hwan Mook Kim
Molecular Pharmacology March 2006, 69 (3) 941-949; DOI: https://doi.org/10.1124/mol.105.017442
Jong Soon Kang
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Yeo Dae Yoon
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Mi Hwa Han
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Sang-Bae Han
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Kiho Lee
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Ki Hoon Lee
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Song-Kyu Park
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Hwan Mook Kim
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Abstract

(R)-4-(3,4-Dihydro-8,8-dimethyl)-2H,8H-benzo[1,2-b:3,4-b′] dipyran-3yl)-1,3-benzenediol (glabridin) is known to have anti-inflammatory, antimicrobial, and cardiovascular protective activities. In the present study, we report the inhibitory effect of glabridin on intercellular adhesion molecule-1 (ICAM-1) expression in tumor necrosis factor-α (TNF-α)-stimulated human umbilical vein endothelial cells (HUVECs). Glabridin inhibited THP-1 cell adhesion to HUVECs stimulated by TNF-α and cell surface expression of ICAM-1 in TNF-α-stimulated HUVECs. The mRNA expression of adhesion molecules, including ICAM-1, vascular cell adhesion molecule-1, and E-selectin, was also suppressed by glabridin. Further study demonstrated the inhibitory effect of glabridin on nuclear factor (NF)-κB/Rel DNA binding, inhibitory factor-κBα (IκBα), and IκBβ degradation, IκB kinase activation, and p65 nuclear translocation in TNF-α-stimulated HUVECs. Treatment of a variety of cell lines with glabridin revealed that inhibitory effect of glabridin on NF-κB/Rel activation is not cell type-specific, and both inducible and constitutive NF-κB/Rel activation was suppressed by glabridin treatment. Moreover, TNF-α-induced phosphorylation of Akt and extracellular signal-regulated kinase (ERK) was blocked by glabridin treatment in HUVECs. Glabridin also suppressed sphingosine-1-phosphate (S1P)-induced cell surface expression and mRNA expression of ICAM-1. Further study demonstrated that TNF-α-induced sphingosine kinase activity was inhibited by glabridin, and the inhibitory effect of glabridin on TNF-α-induced ICAM-1 expression was reversed by addition of exogenous S1P. Together, our results indicate that the inhibitory effect of glabridin on ICAM-1 expression might be mediated, at least in part, by inhibiting sphingosine kinase pathway and subsequent inhibition of signaling pathways, including Akt, ERK, and NF-κB/Rel signaling pathway.

  • Received July 28, 2005.
  • Accepted December 14, 2005.
  • The American Society for Pharmacology and Experimental Therapeutics
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Molecular Pharmacology: 69 (3)
Molecular Pharmacology
Vol. 69, Issue 3
1 Mar 2006
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Glabridin Suppresses Intercellular Adhesion Molecule-1 Expression in Tumor Necrosis Factor-α-Stimulated Human Umbilical Vein Endothelial Cells by Blocking Sphingosine Kinase Pathway: Implications of Akt, Extracellular Signal-Regulated Kinase, and Nuclear…
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Research ArticleArticle

Glabridin Suppresses Intercellular Adhesion Molecule-1 Expression in Tumor Necrosis Factor-α-Stimulated Human Umbilical Vein Endothelial Cells by Blocking Sphingosine Kinase Pathway: Implications of Akt, Extracellular Signal-Regulated Kinase, and Nuclear Factor-κB/Rel Signaling Pathways

Jong Soon Kang, Yeo Dae Yoon, Mi Hwa Han, Sang-Bae Han, Kiho Lee, Ki Hoon Lee, Song-Kyu Park and Hwan Mook Kim
Molecular Pharmacology March 1, 2006, 69 (3) 941-949; DOI: https://doi.org/10.1124/mol.105.017442

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Research ArticleArticle

Glabridin Suppresses Intercellular Adhesion Molecule-1 Expression in Tumor Necrosis Factor-α-Stimulated Human Umbilical Vein Endothelial Cells by Blocking Sphingosine Kinase Pathway: Implications of Akt, Extracellular Signal-Regulated Kinase, and Nuclear Factor-κB/Rel Signaling Pathways

Jong Soon Kang, Yeo Dae Yoon, Mi Hwa Han, Sang-Bae Han, Kiho Lee, Ki Hoon Lee, Song-Kyu Park and Hwan Mook Kim
Molecular Pharmacology March 1, 2006, 69 (3) 941-949; DOI: https://doi.org/10.1124/mol.105.017442
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