Nomura M, Ma W, Chen N, Bode A M, Dong Z
The Hormel Institute, University of Minnesota, 801 16th Avenue NE, Austin, MN 55912, USA.
Carcinogenesis. 2000 Oct;21(10):1885-90. doi: 10.1093/carcin/21.10.1885.
(-)-Epigallocatechin gallate (EGCG) and theaflavins are believed to be the key active components in tea for the chemoprevention of cancer. However, the molecular mechanisms by which EGCG and theaflavins block carcinogenesis are not clear. In the JB6 mouse epidermal cell line a tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA), which causes cell transformation at high frequency, markedly induced NF-kappaB activation. We found that EGCG and theaflavins inhibited TPA-induced NF-kappaB activity in a concentration-dependent manner. These polyphenols blocked TPA-induced phosphorylation of IkappaBalpha at Ser32 in the same concentration range. Moreover, the NF-kappaB sequence-specific DNA-binding activity induced by TPA was also inhibited by these polyphenols. These results suggest that inhibition of NF-kappaB activation is also important in accounting for the anti-tumor promotion effects of EGCG and theaflavins.
（-）-表没食子儿茶素没食子酸酯（EGCG）和茶黄素被认为是茶叶中用于癌症化学预防的关键活性成分。然而，EGCG和茶黄素阻断致癌作用的分子机制尚不清楚。在JB6小鼠表皮细胞系中，一种能高频诱导细胞转化的肿瘤促进剂12-O-十四酰佛波醇-13-乙酸酯（TPA）可显著诱导NF-κB激活。我们发现EGCG和茶黄素以浓度依赖的方式抑制TPA诱导的NF-κB活性。这些多酚在相同浓度范围内阻断了TPA诱导的IκBα在Ser32处的磷酸化。此外，TPA诱导的NF-κB序列特异性DNA结合活性也被这些多酚抑制。这些结果表明，抑制NF-κB激活在解释EGCG和茶黄素的抗肿瘤促进作用中也很重要。
