(-)-Epigallocatechin-3-gallate potentiates the cytotoxicity induced by benzyl isothiocyanate and hydrogen peroxide in human Jurkat T lymphocytes.
(-)-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 H(2)O(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.
Wu
Haitao
H
Graduate School of Natural Science and Technology, Okayama University, Japan.
Yokoyama
Tomoko
T
Zhu
Beiwei
B
Shimoishi
Yasuaki
Y
Murata
Yoshiyuki
Y
Nakamura
Yoshimasa
Y
D017209:Apoptosis / Q000187:drug effects; D002392:Catechin / Q000031:analogs & derivatives* / Q000494:pharmacology; D006801:Humans; D006861:Hydrogen Peroxide / Q000633:toxicity*; D017879:Isothiocyanates / Q000633:toxicity*; D019169:Jurkat Cells; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D013601:T-Lymphocytes / Q000187:drug effects* / Q000378:metabolism
D017879:Isothiocyanates; C031403:benzyl isothiocyanate; D002392:Catechin; D006861:Hydrogen Peroxide; C045651:epigallocatechin gallate; D020928:Mitogen-Activated Protein Kinases