大黄素对人肝癌SMMC7721细胞增殖的抑制作用
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篇名: | 大黄素对人肝癌SMMC7721细胞增殖的抑制作用 |
TITLE: | |
摘要: | 目的:研究大黄素对人肝癌SMMC7721细胞增殖的抑制作用。方法:以0(阴性对照)、25、37.5、50、62.5、75、87.5、100 μmol/L大黄素溶液和100 μmol/L 5-氟尿嘧啶(5-FU)培养SMMC7721细胞24、48、72 h,检测细胞光密度,计算增殖抑制率。以0(阴性对照)、25、50、75 μmol/L大黄素溶液和100 μmol/L 5-FU培养SMMC7721细胞48 h,检测细胞凋亡率、周期分布和细胞Bax、B淋巴细胞瘤2(Bcl-2)基因表达。结果:与阴性对照比较,25、37.5、50、62.5、75、87.5、100 μmol/L大黄素溶液和100 μmol/L 5-FU作用后细胞增殖抑制率升高,且与大黄素的浓度和作用时间呈正相关。与阴性对照比较,25、50、75 μmol/L大黄素和100 μmol/L 5-FU作用后细胞凋亡率升高、Bax基因表达增强、Bcl-2基因表达减弱,其中50、75 μmol/L大黄素溶液和100 μmol/L 5-FU能明显滞留细胞于G0/G1期(P<0.05或P<0.01)。结论:大黄素能抑制SMMC7721细胞增殖,促进其凋亡,阻止其生长。 |
ABSTRACT: | OBJECTIVE: To study the inhibitory effects of emodin on the proliferation of human hepatocellular carcinoma SMMC7721 cells. METHODS: SMMC7721 cells were treated with 0 (negative control), 25, 37.5, 50, 62.5, 75, 87.5, 100 μmol/L emodin solution and 100 μmol/L 5-FU for 24 h, 48 h, 72 h. The optical density value of cells was detected, and inhibition rate was calculated. SMMC7721 cells were treated with 0 (negative control), 25, 50, 75 μmol/L emodin solution and 100 μmol/L 5-FU for 48 h, and cell apoptosis rate, cell cycle and the expression of Bax and Bcl-2 gene were detected. RESULTS: Compared with negative control, the rate of cell proliferation inhibition increased after treated with 25, 37.5, 50, 62.5, 75, 87.5, 100 μmol/L emodin and 100 μmol/L 5-FU, which was positively associated with the concentration and duration. Compared with negative control, the rate of cell apoptosis increased after treated with 25, 50, 75 μmol/L emodin solution and 100 μmol/L 5-FU; the expression of Bax increased and that of Bcl-2 dereased; 50, 75 μmol/L emodin solution and 100 μmol/L 5-FU could arrested cells at G0/G1 phase (P<0.05 or P<0.01). CONCLUSIONS: Emodin can inhibit the proliferation of SMMC7721, promote cell apoptosis and inhibit cell growth. |
期刊: | 2016年第27卷第1期 |
作者: | 王昕雯,朱国光 |
AUTHORS: | WANG Xinwen,ZHU Guoguang |
关键字: | 大黄素;人肝癌SMMC7721细胞;Bax;B淋巴细胞瘤-2;细胞周期;凋亡 |
KEYWORDS: | Emodin; Human hepatocellular carcinoma SMMC7721 cells; Bax; Bcl-2; Cell cycle; Apoptosis |
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