Induction of apoptosis by epigallocatechin-3-gallate in human lymphoblastoid B cells
- Department of Nutrition Management, Faculty of Health Science, Hyogo University, Kakogawa, Hyogo 675-0101 (Japan)
- Department of Genomic Science, Kobe University Graduate School of Medicine, Kobe, Hyogo 650-0017 (Japan)
- Division of Biochemistry, Faculty of Pharmaceutical Sciences, Himeji Dokkyo University, Himeji, Hyogo 670-8524 (Japan)
- Department of Laboratory Medicine, Kawasaki Medical School, Kurashiki, Okayama 701-0192 (Japan)
(-)-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.
- OSTI ID:
- 21032952
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 362, Issue 4; Other Information: DOI: 10.1016/j.bbrc.2007.08.079; PII: S0006-291X(07)01809-8; Copyright (c) 2007 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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