Japanese Green Tea as a Cancer Preventive in Humans
Fujiki Hirota, Suganuma Masami, Okabe Sachiko, Komori Atsumasa, Sueoka Eisaburo, Sueoka Naoko, Kozu Tomoko, Sakai Yuzo,
소속 상세정보
( Fujiki Hirota )
일본 Saitama Cancer Center Research Institute
( Suganuma Masami )
일본 Saitama Cancer Center Research Institute
( Okabe Sachiko )
일본 Saitama Cancer Center Research Institute
( Komori Atsumasa )
일본 Saitama Cancer Center Research Institute
( Sueoka Eisaburo )
일본 Saitama Cancer Center Research Institute
( Sueoka Naoko )
일본 Saitama Cancer Center Research Institute
( Kozu Tomoko )
일본 Saitama Cancer Center Research Institute
( Sakai Yuzo )
일본 Saitama Cancer Center Research Institute
KMID : 0603519970020020083
Abstract
Drinking green tea today is part of Japanese culture. The tea plant Camellia sinenses was imported by a japanese Zen priest in the 12th century from China to Japan as a medicine. However, as a medicine, tea was not much studied. At present we drink tea during and after meals, that is, throughout the day. One cup of green tea infusion contains about 100 ∼ 200 mg of tannins, the main constituent of which is ( - )-epigallocatechin gallate (EGCG). Thus, EGCG is one of the tea polyphenols or tea tannins. In 1983 we did the first scientific examination of EGCG as a cancer-preventive material in collaboration with Takuo Okuda, who was a professor of pharmacology at Okayama University at that time. We began with a study of the anticarcinogenic effects of polyphenols derived from medicinal plants and drugs. We first examined whether a polyphenol shared the phorbol ester receptor with a tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA). Experimentally, EGCG inhibited in a dose-dependent manner the specific 3H-TPA binding to the phorbol ester receptor in a membrane fraction of mouse skin. The median effective dose (ED50) of EGCG for inhibition was about 300 times less than that of TPA. Moreover, penta-O-galloyl-β-D-glucose isolated from a gall, Shisandrea fructus, pedunculagin, chebulinic acid, and buddledin A bound to the same receptors with similar ED50 values as EGCG did, although their structures are related neither to
that of TPA nor to each other. These results raised a question: Does EGCG act as an antagonist, inhibiting the action of TPA, or as an agonist, activating protein kinase C as TPA does? We found that EGCG dose dependently inhibited the activation of protein kinase C induced by teleocidin, which is one of the TPA-type tumor promoters and a new activator of protein kinase C. In 1987 we first reported that EGCG acted af an antagonist and inhibited tumor promotion of teleocidin in a two-stage carcinogenesis experiment on mouse skin.
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