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Inhibition of Ultraviolet B–Induced AP‐1 Activation by Theaflavins From Black Tea
Author(s) -
Nomura Masaaki,
Ma WeiYa,
Huang Chuanshu,
Yang Chung S.,
Bowden G. Tim,
Miyamoto Kenichi,
Dong Zigang
Publication year - 2000
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/1098-2744(200007)28:3<148::aid-mc3>3.0.co;2-q
Subject(s) - polyphenol , epigallocatechin gallate , tumor promotion , black tea , activator (genetics) , biology , kinase , extracellular , transcription factor , mapk/erk pathway , inhibitory postsynaptic potential , protein kinase a , biochemistry , pharmacology , endocrinology , food science , gene , carcinogenesis , antioxidant
Theaflavins are believed to be key active components in black tea for chemoprevention of cancer. However, the molecular mechanisms underlying the inhibitory effects of theaflavins are not clear. With the JB6 mouse epidermal cell line, we investigated the effects of theaflavins on ultraviolet (UV) B radiation–induced activator protein‐1 (AP‐1)–dependent transcriptional activation and compared them with (−)‐epigallocatechin‐3‐gallate (EGCG), a major green tea polyphenol that has cancer chemopreventative activity. Theaflavins and EGCG inhibited UVB‐induced AP‐1 activation in a concentration‐dependent manner. The inhibitory effects of theaflavins were stronger than those of EGCG. We found that theaflavins significantly inhibited activation of extracellular signal‐regulated protein kinases and c‐jun NH 2 ‐terminal kinases. Because the transcription factor AP‐1 is important in the process of tumor promotion, the inhibitory effect of these polyphenols on AP‐1 activation may further explain the anti–tumor promotion action of these tea constituents. Mol. Carcinog. 28:148–155, 2000. © 2000 Wiley‐Liss, Inc.