(−)-Epigallocatechin-3-gallate Potentiates the Cytotoxicity Induced by Benzyl Isothiocyanate and Hydrogen Peroxide in Human Jurkat T Lymphocytes

Haitao WU; Tomoko YOKOYAMA; Beiwei ZHU; Yasuaki SHIMOISHI; Yoshiyuki MURATA; Yoshimasa NAKAMURA

doi:10.1271/bbb.80422

This article has now been updated. Please use the final version.

(−)-Epigallocatechin-3-gallate Potentiates the Cytotoxicity Induced by Benzyl Isothiocyanate and Hydrogen Peroxide in Human Jurkat T Lymphocytes

Haitao WU, Tomoko YOKOYAMA, Beiwei ZHU, Yasuaki SHIMOISHI, Yoshiyuki MURATA, Yoshimasa NAKAMURA

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Keywords: (−)-epigallocatechin-3-gallate (EGCG), extracellular signal-regulated protein kinase (ERK), c-jun N-terminal kinase (JNK), apoptosis, Jurkat cells

JOURNAL FREE ACCESS Advance online publication

Article ID: 80422

DOI https://doi.org/10.1271/bbb.80422

The final version of this article is now available: Vol. 72 (2008) , No. 11 p.3034

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Abstract

(−)-Epigallocatechin-3-gallate (EGCG)-induced apoptosis was along both the extracellular signal-regulated protein kinase (ERK) and c-jun N-terminal kinase (JNK) pathways in Jurkat cells. Co-treatment with EGCG potentiated the cytotoxicity induced by benzyl isothiocyanate (BITC) and H₂O₂, both being inhibited by ERK and JNK inhibitors. These results suggest the significant role of mitogen-activated protein kinase (MAPK) signaling in the apoptosis induction regulated by EGCG alone and in combination.

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