(-)-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

(-)-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

School of Agriculture

Research output: Contribution to journal › Article › peer-review

10 Citations (Scopus)

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 H₂O ₂, 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.

Original language	English
Pages (from-to)	3034-3037
Number of pages	4
Journal	Bioscience, Biotechnology and Biochemistry
Volume	72
Issue number	11
DOIs	https://doi.org/10.1271/bbb.80422
Publication status	Published - 2008

Keywords

(-)-epigallocatechin-3-gallate (EGCG)
Apoptosis
Extracellular signal-regulated protein kinase (ERK)
Jurkat cells
c-jun N-terminal kinase (JNK)

ASJC Scopus subject areas

Biotechnology
Analytical Chemistry
Biochemistry
Applied Microbiology and Biotechnology
Molecular Biology
Organic Chemistry

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10.1271/bbb.80422

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title = "(-)-Epigallocatechin-3-gallate potentiates the cytotoxicity induced by benzyl isothiocyanate and hydrogen peroxide in human Jurkat T lymphocytes",

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 H2O 2, 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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T1 - (-)-Epigallocatechin-3-gallate potentiates the cytotoxicity induced by benzyl isothiocyanate and hydrogen peroxide in human Jurkat T lymphocytes

AU - Wu, Haitao

AU - Yokoyama, Tomoko

AU - Zhu, Beiwei

AU - Shimoishi, Yasuaki

AU - Murata, Yoshiyuki

AU - Nakamura, Yoshimasa

PY - 2008

Y1 - 2008

N2 - (-)-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 H2O 2, 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.

AB - (-)-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 H2O 2, 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.

KW - (-)-epigallocatechin-3-gallate (EGCG)

KW - Apoptosis

KW - Extracellular signal-regulated protein kinase (ERK)

KW - Jurkat cells

KW - c-jun N-terminal kinase (JNK)

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JO - Bioscience, Biotechnology and Biochemistry

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ER -

(-)-Epigallocatechin-3-gallate potentiates the cytotoxicity induced by benzyl isothiocyanate and hydrogen peroxide in human Jurkat T lymphocytes

Abstract

Keywords

ASJC Scopus subject areas

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