以Sephadex LH-20柱色谱分离得到茶黄素双没食子酸酯(TFDG)成分,以H1299和HCT-116细胞分析了该成分的抗癌活性及其作用机理。结果表明,TFDG具有良好的抑制H1299细胞生长的活性,IC50为25μmol/L;有调节细胞周期的活性,可增加HCT-116细胞G1期细胞的比例;有促进HCT-116细胞凋亡的作用,浓度为50μmol/L时效果显著,48βh凋亡率达到40%以上;Western杂交技术分析结果表明,它可降低HCT-116细胞中促癌蛋白质因子Bcl-xL的表达量,可增加抑癌蛋白质因子Bax的表达量。
Theaflavin digallate was purified by Sephadex LH-20 column chromatography. Its anticancer activity and mechanism were analyzed on H1299 and HCT-116 cancer cell lines. Results from MTT assay showed that Theaflavin digallate could inhibit the growth of H1299, and its IC50 value is 25μmol/L. Theaflavin digallate could slightly adjust the cell cycle of HCT-116 cancer cell, and significantly promote the apoptosis of HCT-116 cancer cell at 50μmol/L. Theaflavin digallagte could decrease the expression of cancer-promoting biomarker, Bcl-xL, and increase the expression of cancer-inhibiting biomarker, Bax, on HCT-116 cancer cell line.
[1] 江和源, 程启坤, 杜琪珍, 等. 红茶中的茶黄素[J]. 中国茶叶, 1998, 20(3): 18~20.
[2] 程启坤. 红茶中的茶黄素[J]. 国外农学──茶叶, 1983(1): 1~14.
[3] 陈宗懋. 茶对人体的生理调节机能[J]. 茶叶文摘, 1994 (1): 1~8, (2): 1~9.
[4] 杜琪珍, 江和源. 茶色素的药理及其功效[J]. 中国茶叶, 199719(5): 42~43.
[5] Collier PD, Bryce T, Mallows R, et al. The Theaflavins of Black Tea[J]. Tetrahedon., 1973, 29: 125~142.
[6] 江和源, 程启坤, 杜琪珍. 高速逆流色谱在茶黄素分离上的应用[J]. 茶叶科学, 2000, 20(1): 40~44.
[7] Yu-Chih Liang, Yen-Chou Chen, Yu-Li Lin, et al. Suppression of extracellular signals and cell proliferation by the black tea polyphenol, theaflavin-3,3’-digallate[J]. Carcinogenesis, 1999, 20(4): 733~736.
[8] Mou-Tan Huang, Yue Liu, Divya Ramji, et al. Inhibitory effects of black tea theaflavin derivatives on 12-O-tetradecanoylphorbol-13-acetate-induced inflammation and arachidonic acid metabolism in mouse ears[J]. Mol. Nutr Food Res, 2006, 50: 115~122.
[9] Nicholas J.M, Cinzia C, Lilian T, et al. The antioxidant properties of theaflavins and their gallate esters-radical scavengers or metal chelators[J]. FEBS Letters, 1996, 392: 40~44.
[10] Hideya Mizuno, Yong-Yeon Cho, Feng Zhu, et al. Theaflavin-3,3’-digallate induces epidermal growth factor receptor downregulation[J]. Molecular Carcinogenesis, 2006, 45: 204~212.