Uesato S, Kitagawa Y, Kamishimoto M, Kumagai A, Hori H, Nagasawa H
Department of Biotechnology, Faculty of Engineering, Kansai University, Suita, 564-8680, Osaka, Japan.
Cancer Lett. 2001 Sep 10;170(1):41-4. doi: 10.1016/s0304-3835(01)00571-7.
The ability of (-)-epicatechin (EC), (-)-epigallocatechin (EGC) and (-)-epigallocatechin gallate (EGCG) to inhibit the growth of HCT 116 colorectal and Hep G2 hepatocellular carcinoma cells was examined by MTT and clonogenic assays (CA). The respective catechins inhibited the growth of HCT 116 more strongly than Hep G2. In MTT assay, IC(50) values of EGC and EGCG against HCT 116 grew smaller on prolongation of the exposure times of the cells to the catechins. In CA, however, these two catechins had IC(50) values ranging between 7.6+/-0.4 and 11.2+/-0.5 microM against the same cells regardless of the exposure times. EC showed much weaker growth inhibitions relative to the two aforementioned catechins.
通过MTT和克隆形成试验(CA)检测了(-)-表儿茶素(EC)、(-)-表没食子儿茶素(EGC)和(-)-表没食子儿茶素没食子酸酯(EGCG)抑制HCT 116结肠癌细胞和Hep G2肝癌细胞生长的能力。与Hep G2相比,各儿茶素对HCT 116细胞生长的抑制作用更强。在MTT试验中,随着细胞与儿茶素接触时间的延长,EGC和EGCG对HCT 116细胞的半数抑制浓度(IC50)值变小。然而,在克隆形成试验中,无论接触时间如何,这两种儿茶素对相同细胞的IC50值在7.6±0.4至11.2±0.5微摩尔之间。相对于上述两种儿茶素,EC的生长抑制作用弱得多。