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

(−)-Epigallocatechin-3-gallate Potentiates the Cytotoxicity Induced by Benzyl Isothiocyanate and Hydrogen Peroxide in Human Jurkat T Lymphocytes
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(−)-Epigallocatechin-3-gallate 增强异硫氰酸苄酯和过氧化氢对人 Jurkat T 淋巴细胞诱导的细胞毒性

DOI:
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发表时间:
2008
期刊:
Bioscience, biotechnology and biochemistry
影响因子:
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通讯作者:
Yoshimasa Nakamura
Yoshimasa Nakamura
中科院分区:
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文献类型:
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作者:
Haitao Wu;T. Yokoyama;B. Zhu;Y. Shimoishi;Y. Murata;Yoshimasa Nakamura

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(−)-表没食子儿茶素没食子酸酯(EGCG)诱导的Jurkat细胞凋亡沿着细胞外信号调节蛋白激酶(ERK)和c-jun N-末端激酶(JNK)途径。与EGCG共处理增强了异硫氰酸苄酯(BITC)和H2 O2诱导的细胞毒性,ERK和JNK抑制剂均抑制。这些结果表明,有丝分裂原活化蛋白激酶(MAPK)信号转导的重要作用,在细胞凋亡的诱导由表没食子儿茶素没食子酸酯单独和组合调节。
(−)-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.
DOI: 10.1016/j.bcp.2008.02.016
发表时间: 2008-05-15
影响因子: 5.8
作者:
Kim, Young-Ho;Lee, Dae-Hee;Lee, Yong J.
通讯作者: Lee, Yong J.