Tea catechins inhibit cell proliferation through hydrogen peroxide-dependent and -independent pathways in human T lymphocytic leukemia Jurkat cells

Yue Tang, Naomi Abe, Hang Qi, Beiwei Zhu, Yoshiyuki Murata, Yoshimasa Nakamura

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

In the present study, we investigated the anti-proliferative effects of four tea catechins: (-)-epicatechin (EC), (-)-epigallocatechin (EGC), (-)-epicatechin gallate (ECg) and (-)-epigallocatechin gallate (EGCg) in human T lymphocytic leukemia Jurkat cells. Each catechin induced a significant cytotoxic effect on Jurkat cells. Combinations of EGCg with other catechins additively potentiated anti-proliferation, extracellular hydrogen peroxide formation, c-Jun N-terminal kinase (JNK) activation and interferon (IFN)-γ mRNA expression. Catalase partly but significantly abolished the cytotoxicity induced by EGC or EGCg, whereas it did not influence the EC- or ECg-induced effect. Among the tea catechins, ECg synergistically enhanced the EGCg-induced JNK phosphorylation and IFN-γ expression. The present findings provide evidence that tea catechins are able to concertedly induce cytotoxicity through the JNK/IFN-γ pathway in both a hydrogen peroxide-dependent and -independent manner.

Original languageEnglish
Pages (from-to)1245-1249
Number of pages5
JournalFood Science and Technology Research
Volume20
Issue number6
DOIs
Publication statusPublished - 2014

Fingerprint

Interferons
T-Cell Leukemia
lymphocytic leukemia
Jurkat Cells
Catechin
epigallocatechin
Cell proliferation
Tea
flavanols
Hydrogen peroxide
Hydrogen Peroxide
tea
epicatechin
hydrogen peroxide
cell proliferation
Cell Proliferation
Cytotoxicity
interferons
cytotoxicity
Phosphorylation

Keywords

  • c-Jun N-terminal kinase
  • Cytotoxicity
  • Hydrogen peroxide
  • Interferon-γ
  • Jurkat cells
  • Tea catechins

ASJC Scopus subject areas

  • Food Science
  • Industrial and Manufacturing Engineering
  • Chemical Engineering(all)
  • Biotechnology
  • Marketing

Cite this

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abstract = "In the present study, we investigated the anti-proliferative effects of four tea catechins: (-)-epicatechin (EC), (-)-epigallocatechin (EGC), (-)-epicatechin gallate (ECg) and (-)-epigallocatechin gallate (EGCg) in human T lymphocytic leukemia Jurkat cells. Each catechin induced a significant cytotoxic effect on Jurkat cells. Combinations of EGCg with other catechins additively potentiated anti-proliferation, extracellular hydrogen peroxide formation, c-Jun N-terminal kinase (JNK) activation and interferon (IFN)-γ mRNA expression. Catalase partly but significantly abolished the cytotoxicity induced by EGC or EGCg, whereas it did not influence the EC- or ECg-induced effect. Among the tea catechins, ECg synergistically enhanced the EGCg-induced JNK phosphorylation and IFN-γ expression. The present findings provide evidence that tea catechins are able to concertedly induce cytotoxicity through the JNK/IFN-γ pathway in both a hydrogen peroxide-dependent and -independent manner.",
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TY - JOUR

T1 - Tea catechins inhibit cell proliferation through hydrogen peroxide-dependent and -independent pathways in human T lymphocytic leukemia Jurkat cells

AU - Tang, Yue

AU - Abe, Naomi

AU - Qi, Hang

AU - Zhu, Beiwei

AU - Murata, Yoshiyuki

AU - Nakamura, Yoshimasa

PY - 2014

Y1 - 2014

N2 - In the present study, we investigated the anti-proliferative effects of four tea catechins: (-)-epicatechin (EC), (-)-epigallocatechin (EGC), (-)-epicatechin gallate (ECg) and (-)-epigallocatechin gallate (EGCg) in human T lymphocytic leukemia Jurkat cells. Each catechin induced a significant cytotoxic effect on Jurkat cells. Combinations of EGCg with other catechins additively potentiated anti-proliferation, extracellular hydrogen peroxide formation, c-Jun N-terminal kinase (JNK) activation and interferon (IFN)-γ mRNA expression. Catalase partly but significantly abolished the cytotoxicity induced by EGC or EGCg, whereas it did not influence the EC- or ECg-induced effect. Among the tea catechins, ECg synergistically enhanced the EGCg-induced JNK phosphorylation and IFN-γ expression. The present findings provide evidence that tea catechins are able to concertedly induce cytotoxicity through the JNK/IFN-γ pathway in both a hydrogen peroxide-dependent and -independent manner.

AB - In the present study, we investigated the anti-proliferative effects of four tea catechins: (-)-epicatechin (EC), (-)-epigallocatechin (EGC), (-)-epicatechin gallate (ECg) and (-)-epigallocatechin gallate (EGCg) in human T lymphocytic leukemia Jurkat cells. Each catechin induced a significant cytotoxic effect on Jurkat cells. Combinations of EGCg with other catechins additively potentiated anti-proliferation, extracellular hydrogen peroxide formation, c-Jun N-terminal kinase (JNK) activation and interferon (IFN)-γ mRNA expression. Catalase partly but significantly abolished the cytotoxicity induced by EGC or EGCg, whereas it did not influence the EC- or ECg-induced effect. Among the tea catechins, ECg synergistically enhanced the EGCg-induced JNK phosphorylation and IFN-γ expression. The present findings provide evidence that tea catechins are able to concertedly induce cytotoxicity through the JNK/IFN-γ pathway in both a hydrogen peroxide-dependent and -independent manner.

KW - c-Jun N-terminal kinase

KW - Cytotoxicity

KW - Hydrogen peroxide

KW - Interferon-γ

KW - Jurkat cells

KW - Tea catechins

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