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作 者:王帅[1] 尚志梅[1] 黄利敏[1] 刘亮[2] 武中林[2] 赵阳[2] 祝敬燕[1]
机构地区:[1]潍坊市中医院肿瘤三科,山东潍坊261041 [2]河北医科大学第四医院肿瘤所,石家庄050011
出 处:《解放军医学杂志》2016年第3期199-203,共5页Medical Journal of Chinese People's Liberation Army
摘 要:目的探讨表没食子儿茶素没食子酸酯(EGCG)对肝癌细胞Hep G2增殖和凋亡的影响及其可能机制。方法采用不同浓度(0、25、50、100、200、400mg/L)EGCG作用于Hep G2细胞,于24、48h后采用MTT方法检测细胞增殖抑制率。以不同浓度(0、50、100、200mg/L)EGCG作用于Hep G2细胞,24h后采用流式细胞术检测细胞凋亡率、细胞周期、细胞分裂周期蛋白25A(CDC25A)及Smad3蛋白的表达,RT-PCR检测CDC25A和Smad3 m RNA的表达。结果MTT检测结果显示,不同浓度EGCG对Hep G2细胞均有生长抑制作用,且具有时间和剂量依赖性(P<0.01)。随着EGCG浓度升高,细胞增殖指数(PI)明显降低(P<0.01),细胞凋亡率明显增高(P<0.01),CDC25A蛋白和m RNA表达水平下降(P<0.05),Smad3蛋白和m RNA表达水平上升(P<0.05)。结论 EGCG可能通过下调CDC25A、上调Smad3的表达,抑制Hep G2细胞增殖并诱导其凋亡,从而对肝癌细胞起到生长抑制作用。Objective To study the effect of epigallocatechin-3-gallate(EGCG) on the proliferation and apoptosis of hepatic carcinoma Hep G2 cells, and to explore the possible mechanism. Methods Hep G2 cells were treated with EGCG in various concentrations(0, 25, 50, 100, 200, 400mg/L) for 24, 48 and 72 h, and then the cell proliferation inhibition rate was determined with MTT. Again, the Hep G2 cells were treated with various concentrations of EGCG(0, 50, 100, 200mg/L) for 24 h, and then the cell apoptosis rate, cell cycle, and the expressions of cell division cycle protein 25A(CDC25A), and Smad3 protein were determined with flow cytometry. m RNA expressions of CDC25 A and Smad3 were assessed with RT-PCR. Results The results of MTT showed that various concentrations of EGCG inhibited the growth of Hep G2 cells in dose and time dependent manner(P〈0.01). The result of flow cytometry showed that, with the increase of of EGCG concentration, the cell proliferation index(PI) decreased significantly(P〈0.01), while the apoptosis rate increased obviously(P〈0.01); the expression levels of CDC25 A protein and m RNA decreased(P〈0.05) and of Smad3 protein and m RNA increased(P〈0.05). Conclusion EGCG may play a role in growth inhibition of hepatic carcinoma cells by down-regulating the expression of CDC25 A, up-regulating the expression of Smad3, thus inhibiting proliferation and inducing apoptosis of Hep G2 cells.
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