Induction of apoptosis by epigallocatechin-3-gallate in human lymphoblastoid B cells
| Autor: | Tomoko Takano, Yumi Tohyama, Chisato Tanaka, Hirohei Yamamura, Kaoru Tohyama, Chiseko Noda, Jinsong He, Toshinori Kondo |
|---|---|
| Rok vydání: | 2007 |
| Předmět: |
Lymphoma
B-Cell Cell Survival Biophysics Antineoplastic Agents Apoptosis Mitochondrion medicine.disease_cause complex mixtures Biochemistry Catechin Cell Line medicine Humans heterocyclic compounds Molecular Biology chemistry.chemical_classification Reactive oxygen species Dose-Response Relationship Drug biology Cell growth Cytochrome c food and beverages Cell Biology Cell biology Cytosol chemistry Cell culture biology.protein sense organs Apoptosis Regulatory Proteins Reactive Oxygen Species Oxidative stress Signal Transduction |
| Zdroj: | Biochemical and Biophysical Research Communications. 362:951-957 |
| ISSN: | 0006-291X |
| DOI: | 10.1016/j.bbrc.2007.08.079 |
| Popis: | (-)-Epigallocatechin-3-gallate (EGCG), a major constituent of green tea polyphenols, has been shown to suppress cancer cell proliferation and induce apoptosis. In this study we investigated its efficacy and the mechanism underlying its effect using human B lymphoblastoid cell line Ramos, and effect of co-treatment with EGCG and a chemotherapeutic agent on apoptotic cell death. EGCG induced dose- and time-dependent apoptotic cell death accompanied by loss of mitochondrial transmembrane potential, release of cytochrome c into the cytosol, and cleavage of pro-caspase-9 to its active form. EGCG also enhanced production of intracellular reactive oxygen species (ROS). Pretreatment with diphenylene iodonium chloride, an inhibitor of NAD(P)H oxidase and an antioxidant, partially suppressed both EGCG-induced apoptosis and production of ROS, implying that oxidative stress is involved in the apoptotic response. Furthermore, we showed that combined-treatment with EGCG and a chemotherapeutic agent, etoposide, synergistically induced apoptosis in Ramos cells. |
| Databáze: | OpenAIRE |
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