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Inhibition of inducible tumor necrosis factor-alpha expression by the fungal epipolythiodiketopiperazine gliovirin.

Abstract：

:TNF-alpha is a major pro-inflammatory cytokine that regulates further cytokine induction, especially of IL-1 and IL-6, in many human diseases including cancer, inflammation and immune disorders. In a search for new inhibitors of inducible TNF-alpha promoter activity and expression, cultures of the imperfect fungus Trichoderma harzianum were found to produce gliovirin, a previously isolated epipolythiodiketopiperazine. Gliovirin inhibited inducible TNF-alpha promoter activity and synthesis in LPS/IFN-gamma-stimulated macrophages/monocytes and Jurkat T-cells, co-stimulated with 12-O-tetradecanoylphorbol-13-acetate (TPA)/ionomycin, in a dose-dependent manner, with IC(50) values ranging from 0.21 to 2.1 microM (0.1-1 microg/ml). Studies on the mode of action revealed that gliovirin suppresses TNF-alpha synthesis by inhibiting the activation of extracellular signal-regulated kinase (ERK), thereby blocking the pathway leading to activation of the transcription factors AP-1 and NF-kappaB, the latter of which is involved in the inducible expression of many pro-inflammatory genes. Gliovirin also significantly reduced TPA/ionomycin-induced IL-2 mRNA levels and synthesis in Jurkat cells at low micromolar concentrations.

journal_name

Biol Chem

journal_title

Biological chemistry

authors

Rether J,Serwe A,Anke T,Erkel G

doi

10.1515/BC.2007.066

subject

Has Abstract

pub_date

2007-06-01 00:00:00

pages

627-37

issue

6

eissn

1431-6730

issn

1437-4315

journal_volume

388

pub_type

杂志文章

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