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Licochalcone A Potently Inhibits Tumor Necrosis Factor α-Induced Nuclear Factor-κB Activation through the Direct Inhibition of IκB Kinase Complex Activation

Megumi Funakoshi-Tago, Saeko Tanabe, Kenji Tago, Hiroshi Itoh, Tadahiko Mashino, Yoshiko Sonoda and Tadashi Kasahara
Molecular Pharmacology October 2009, 76 (4) 745-753; DOI: https://doi.org/10.1124/mol.109.057448
Megumi Funakoshi-Tago
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Saeko Tanabe
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Kenji Tago
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Hiroshi Itoh
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Tadahiko Mashino
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Yoshiko Sonoda
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Tadashi Kasahara
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Abstract

Glycyrrhiza inflata has been used as a traditional medicine with anti-inflammatory activity; however, its mechanism has not been fully understood. Licochalcone A is a major and biogenetically characteristic chalcone isolated from G. inflata. Here, we found that licochalcone A strongly inhibited tumor necrosis (TNF)-α-induced nuclear localization, DNA binding activity, and the transcriptional activity of nuclear factor-κB (NF-κB). Whereas licochalcone A had no effect on the recruitment of receptor-interacting protein 1 and IκB kinase β (IKKβ) to TNF receptor I by TNF-α, it significantly inhibited TNF-α-induced IκB kinase complex (IKK) activation and inhibitor of nuclear factor-κB degradation. It is interesting that we found that the cysteine residue at position 179 of IKKβ is essential for licochalcone A-induced IKK inhibition, because licochalcone A failed to affect the kinase activity of the IKKβ (C179A) mutant. In contrast, a structurally related compound, echinatin, failed to inhibit TNF-α-induced IKK activation and NF-κB activation, suggesting that the 1,1-dimethy-2-propenyl group in licochalcone A is important for the inhibition of NF-κB. In addition, TNF-α-induced expression of inflammatory cytokines CCL2/monocyte chemotactic protein-1and CXCL1/KC was clearly inhibited by licochalcone A but not echinatin. Taken together, licochalcone A might contribute to the potent anti-inflammatory effect of G. inflata through the inhibition of IKK activation.

  • TNF, tumor necrosis factor
  • MCP, monocyte chemotactic protein
  • NF-κB, nuclear factor-κB
  • IKK, IκB kinase complex
  • IκBα, inhibitor of nuclear factor-κB
  • TNFR, tumor necrosis factor receptor
  • TRADD, tumor necrosis factor receptor-associated death domain
  • RIP, receptor-interacting protein
  • TRAF, tumor necrosis factor receptor-associated factor
  • CMV, cytomegalovirus
  • HEK, human embryonic kidney
  • FBS, fetal bovine serum
  • PBS, phosphate-buffered saline
  • GST, glutathione transferase
  • RT-PCR, reverse transcriptase-polymerase chain reaction
  • GAPDH, glyceraldehyde-3-phosphate dehydrogenase
  • ELISA, enzyme-linked immunosorbent assay
  • DMSO, dimethyl sulfoxide
  • LPS, lipopolysaccharide.

Footnotes

  • This work was supported in part by Ministry of Education, Culture, Sports, Science and Technology Japan [Grants 16390024, 19790071] and the Hi-Tech Research Center Project for Private Universities in Japan.

  • Article, publication date, and citation information can be found at http://molpharm.aspetjournals.org.

  • ABBREVIATIONS:

    • Received May 1, 2009.
    • Accepted July 10, 2009.
  • © 2009 The American Society for Pharmacology and Experimental Therapeutics
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Molecular Pharmacology: 76 (4)
Molecular Pharmacology
Vol. 76, Issue 4
October 2009
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Licochalcone A Potently Inhibits Tumor Necrosis Factor α-Induced Nuclear Factor-κB Activation through the Direct Inhibition of IκB Kinase Complex Activation

Megumi Funakoshi-Tago, Saeko Tanabe, Kenji Tago, Hiroshi Itoh, Tadahiko Mashino, Yoshiko Sonoda and Tadashi Kasahara
Molecular Pharmacology October 1, 2009, 76 (4) 745-753; DOI: https://doi.org/10.1124/mol.109.057448

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Licochalcone A Potently Inhibits Tumor Necrosis Factor α-Induced Nuclear Factor-κB Activation through the Direct Inhibition of IκB Kinase Complex Activation

Megumi Funakoshi-Tago, Saeko Tanabe, Kenji Tago, Hiroshi Itoh, Tadahiko Mashino, Yoshiko Sonoda and Tadashi Kasahara
Molecular Pharmacology October 1, 2009, 76 (4) 745-753; DOI: https://doi.org/10.1124/mol.109.057448
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