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Epigallocatechin-3-Gallate Inhibits Secretion of TNF-α, IL-6 and IL-8 through the Attenuation of ERK and NF-κB in HMC-1 Cells

2006; Karger Publishers; Volume: 142; Issue: 4 Linguagem: Inglês

10.1159/000097503

1423-0097

Hye‐Young Shin, Sang‐Hyun Kim, Hyun‐Ja Jeong, Sang-Yong Kim, Tae‐Yong Shin, Jae‐Young Um, Seung‐Heon Hong, Hyung‐Min Kim,

Phytochemicals and Antioxidant Activities

<i>Background:</i> Epigallocatechin-3-gallate (EGCG) is a major form of tea catechin and has a variety of biological activities. In the present study, we investigated the effect of EGCG on the secretion of TNF-α, IL-6 and IL-8, as well as its possible mechanism of action by using the human mast cell line (HMC-1). <i>Methods:</i> EGCG was treated before the activation of HMC-1 cells with phorbol 12-myristate 13-acetate (PMA) plus calcium ionophore (A23187). To investigate the effect of EGCG on PMA+A23187-stimulated HMC-1 cells, ELISA, Western blot analysis, electrophorectic mobility shift assay and luciferase assay were used in this study. <i>Results:</i> EGCG (100 µ<i>M</i>) inhibited PMA+A23187-induced TNF-α, IL-6 and IL-8 expression and production. EGCG inhibited the intracellular Ca²⁺ level. EGCG attenuated PMA+A23187-induced NF-ĸB and extracellular signal-regulated kinase (ERK1/2) activation, but not that of c-Jun N-terminal kinase or p38 mitogen-activated protein kinase. <i>Conclusion:</i> EGCG inhibited the production of TNF-α, IL-6 and IL-8 through the inhibition of the intracellular Ca²⁺ level, and of ERK1/2 and NF-ĸB activation. These results indicate that EGCG may be helpful in regulating mast-cell-mediated allergic inflammatory response.