Send to

Choose Destination
Int Arch Allergy Immunol. 2007;142(4):335-44. Epub 2006 Nov 29.

Epigallocatechin-3-gallate inhibits secretion of TNF-alpha, IL-6 and IL-8 through the attenuation of ERK and NF-kappaB in HMC-1 cells.

Author information

Department of Pharmacology, College of Oriental Medicine, Institute of Oriental Medicine, Kyung Hee University, Dongdaemun-Gu, Seoul, South Korea.



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-alpha, IL-6 and IL-8, as well as its possible mechanism of action by using the human mast cell line (HMC-1).


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.


EGCG (100 microM) inhibited PMA+A23187-induced TNF-alpha, IL-6 and IL-8 expression and production. EGCG inhibited the intracellular Ca(2+) level. EGCG attenuated PMA+A23187-induced NF-kappaB and extracellular signal-regulated kinase (ERK1/2) activation, but not that of c-Jun N-terminal kinase or p38 mitogen-activated protein kinase.


EGCG inhibited the production of TNF-alpha, IL-6 and IL-8 through the inhibition of the intracellular Ca(2+) level, and of ERK1/2 and NF-kappaB activation. These results indicate that EGCG may be helpful in regulating mast-cell-mediated allergic inflammatory response.

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for S. Karger AG, Basel, Switzerland
Loading ...
Support Center