TY - JOUR
T1 - (-)-epigallocatechin-3-gallate ameliorates photodynamic therapy responses in an in vitro T lymphocyte model
AU - Qi, Hang
AU - Abe, Naomi
AU - Zhu, Beiwei
AU - Murata, Yoshiyuki
AU - Nakamura, Yoshimasa
N1 - Publisher Copyright:
Copyright © 2014 John Wiley & Sons, Ltd.
PY - 2014/10/1
Y1 - 2014/10/1
N2 - (-)-Epigallocatechin-3-gallate (EGCG), the most abundant polyphenolic constituent in green tea, is known as a powerful antioxidant but concomitantly possesses a prooxidant property. We investigated the effect of EGCG on phloxine B (PhB)-induced photocytotoxicity in human T lymphocytic leukemia Jurkat cells. EGCG significantly potentiated PhB-induced photocytotoxic effects, including the inhibition of cell proliferation, DNA fragmentation, and caspase-3 activity induction in Jurkat cells. Catalase attenuated the enhanced cytotoxicity by EGCG, suggesting the involvement of extracellularly produced hydrogen peroxide. Indeed, EGCG significantly enhanced extracellular hydrogen peroxide formation induced by photo-irradiated PhB. The EGCG also enhanced intracellular reactive oxygen species accumulation, c-Jun N-terminal kinase (JNK) phosphorylation, and interferon-γ (IFN-γ) gene expression, all of which are involved in PhB-induced apoptosis. Taken together, our data suggest that EGCG is capable of potentiating photodynamic therapy responses, presumably through the intracellular oxidative stress-sensitive JNK/IFN-γ pathway by exogenous hydrogen peroxide formation.
AB - (-)-Epigallocatechin-3-gallate (EGCG), the most abundant polyphenolic constituent in green tea, is known as a powerful antioxidant but concomitantly possesses a prooxidant property. We investigated the effect of EGCG on phloxine B (PhB)-induced photocytotoxicity in human T lymphocytic leukemia Jurkat cells. EGCG significantly potentiated PhB-induced photocytotoxic effects, including the inhibition of cell proliferation, DNA fragmentation, and caspase-3 activity induction in Jurkat cells. Catalase attenuated the enhanced cytotoxicity by EGCG, suggesting the involvement of extracellularly produced hydrogen peroxide. Indeed, EGCG significantly enhanced extracellular hydrogen peroxide formation induced by photo-irradiated PhB. The EGCG also enhanced intracellular reactive oxygen species accumulation, c-Jun N-terminal kinase (JNK) phosphorylation, and interferon-γ (IFN-γ) gene expression, all of which are involved in PhB-induced apoptosis. Taken together, our data suggest that EGCG is capable of potentiating photodynamic therapy responses, presumably through the intracellular oxidative stress-sensitive JNK/IFN-γ pathway by exogenous hydrogen peroxide formation.
KW - (-)-epigallocatechin-3-gallate
KW - c-Jun N-terminal kinase
KW - interferon-γ
KW - phloxine B
KW - photodynamic therapy
KW - reactive oxygen species
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U2 - 10.1002/ptr.5152
DO - 10.1002/ptr.5152
M3 - Article
C2 - 24700514
AN - SCOPUS:84908556021
SN - 0951-418X
VL - 28
SP - 1486
EP - 1491
JO - Phytotherapy Research
JF - Phytotherapy Research
IS - 10
ER -