Black tea constituents, theaflavins, inhibit 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung tumorigenesis in A/J mice
Black tea constituents, theaflavins, inhibit 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung tumorigenesis in A/J mice
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DOI：
10.1093/carcin/18.12.2361
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发表时间：
1997-12-01
期刊：
影响因子：
4.7
通讯作者：
Yang, CS
中科院分区：
文献类型：
--
作者：
Yang, GY;Liu, ZJ;Yang, CS
在短期研究中，雌性a /J小鼠接受单剂量4-（甲基亚硝胺）-1-（3-吡啶基）-1-丁酮(NNK；在NNK处理24 h后，以0.1和0.3%的茶黄素作为唯一的饮水来源，通过加入溴脱氧尿苷（BrdU）免疫组织化学方法测定肺组织的增殖指数。在第5天观察到，细支气管细胞的增殖率最高，显著降低了0.3%的茶黄素（增殖指数为1.51 +/- 0.08对2.35 +/- 0.16）。在长期的肺肿瘤发生研究中，在NNK治疗后第16周，100%（30/30）的小鼠出现肺腺瘤，从NNK治疗后第2天开始，以茶黄素（0.1%）作为唯一的饮水来源，直到实验结束。显著降低肿瘤的数量和体积，分别减少23% （8.5 +/- 0.6 vs 6.5 +/- 0.6个肿瘤/小鼠）和34% （0.08 vs 0.05 mm(3)个肿瘤/小鼠），茶黄素也显著抑制肺腺瘤的增殖指数，本研究证实了茶黄素对nnk诱导的肺增生和肿瘤发生的抑制作用。
The present study investigated the inhibitory activity against lung tumorigenesis by a group of characteristic black tea polyphenols, theaflavins, In a short-term study, female A/J mice were treated with a single dose of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK; 103 mg/kg b.w., i.p.) on day 0, and 0.1 and 0.3% theaflavins were administered as the sole source of drinking fluid starting 24 h after NNK treatment, The proliferation index of the lung tissues was measured by the incorporation of bromodeoxyuridine (BrdU) immunohistochemically. The highest NNK-induced proliferation rate of bronchiolar cells, observed on day 5, was significantly decreased by 0.3% theaflavins (proliferation index, 1.51 +/- 0.08 versus 2.35 +/- 0.16), In a long-term lung tumorigenesis study, pulmonary adenomas were observed in 100% (30/30) of the mice at week 16 after NNK treatment, Administration of theaflavins (0.1%) as the sole source of drinking fluid, starting 2 days after the NNK treatment until the termination of the experiment, significantly reduced the tumor multiplicity and volume by 23% (8.5 +/- 0.6 versus 6.5 +/- 0.6 tumors/mouse) and 34% (0.08 versus 0.05 mm(3) per tumor), respectively, The proliferation index in lung adenomas was also significantly inhibited by theaflavins, The present work demonstrates the inhibitory action of theaflavins against NNK-induced pulmonary hyperproliferation and tumorigenesis.