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Research ArticleArticle

Gallotannin Inhibits the Expression of Chemokines and Inflammatory Cytokines in A549 Cells

Katalin Erdèlyi, Andrea Kiss, Edina Bakondi, Péter Bai, Csaba Szabó, Pál Gergely, Ferenc Erdödi and László Virág
Molecular Pharmacology September 2005, 68 (3) 895-904; DOI: https://doi.org/10.1124/mol.105.012518
Katalin Erdèlyi
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Andrea Kiss
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Edina Bakondi
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Péter Bai
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Csaba Szabó
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Pál Gergely
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Ferenc Erdödi
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László Virág
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Abstract

Tannins are plant-derived water-soluble polyphenols with wide-ranging biological activities. The mechanisms underlying the anti-inflammatory effect of tannins are not fully understood and may be the result of inhibition of poly(ADP-ribose) (PAR) glycohydrolase (PARG), the main catabolic enzyme of PAR metabolism. Therefore, we set out to investigate the mechanism of the anti-inflammatory effect of gallotannin (GT) in A549 cells with special regard to the role of poly(ADP-ribosyl)ation. Using an inflammation-focused low-density array and reverse transcription-polymerase chain reaction, we found that GT suppressed the expression of most cytokines and chemokines in cytokine-stimulated A549 cells, whereas the PARP inhibitor PJ-34 only inhibited few transcripts. Activation of the transcription factors, nuclear factor κB (NF-κB) and activator protein 1 (AP-1), was blocked by GT, whereas PJ-34 only suppressed NF-κB activation but not AP-1 activation. GT also inhibited IκB phosphorylation and nuclear translocation of NF-κB, but PJ-34 had no effect on these upstream events. In the AP-1 pathway, GT treatment, even in the absence of cytokines, caused maximal phosphorylation of c-Jun N-terminal kinase and c-Jun. GT also caused a low-level phosphorylation of p38, extracellular signal-regulated kinases 1 and 2, activating transcription factor2, and cAMP-response element-binding protein but inhibited cytokine-induced phosphorylation of these kinases and transcription factors. GT inhibited protein phosphatases 1 and 2A, which may explain the increased phosphorylation of mitogen-activated protein kinase and their substrates. GT exerted potent antioxidant effect but failed to cause PAR accumulation. In summary, the potent inhibitory effects of GT on the transcription of cytokine and chemokine genes are probably not related to PARG inhibition. Inhibition of AP-1 activation and upstream signaling events may be responsible for the effects of GT.

  • Received March 3, 2005.
  • Accepted June 20, 2005.
  • The American Society for Pharmacology and Experimental Therapeutics
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Molecular Pharmacology: 68 (3)
Molecular Pharmacology
Vol. 68, Issue 3
1 Sep 2005
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Research ArticleArticle

Gallotannin Inhibits the Expression of Chemokines and Inflammatory Cytokines in A549 Cells

Katalin Erdèlyi, Andrea Kiss, Edina Bakondi, Péter Bai, Csaba Szabó, Pál Gergely, Ferenc Erdödi and László Virág
Molecular Pharmacology September 1, 2005, 68 (3) 895-904; DOI: https://doi.org/10.1124/mol.105.012518

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Research ArticleArticle

Gallotannin Inhibits the Expression of Chemokines and Inflammatory Cytokines in A549 Cells

Katalin Erdèlyi, Andrea Kiss, Edina Bakondi, Péter Bai, Csaba Szabó, Pál Gergely, Ferenc Erdödi and László Virág
Molecular Pharmacology September 1, 2005, 68 (3) 895-904; DOI: https://doi.org/10.1124/mol.105.012518
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