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目的探讨益肾固冲汤抑制乳腺癌细胞增殖,促进其凋亡的作用和抗癌分子的机制。方法体外培养人乳腺细胞株(MCF)-7细胞利用MTT法观察益肾固冲汤对人乳腺癌MCF-7细胞增殖的抑制作用,用流式细胞仪检测益肾固冲汤对人乳腺癌MCF-7凋亡及细胞周期的影响。结果益肾固冲汤对人乳腺癌MCF-7细胞增殖具有抑制作用,都具有明显的时-效和量-效关系。人乳腺癌细胞MCF-7细胞经过不同浓度的益肾固冲汤处理24、48、72 h后,各组均呈现不同程度的凋亡,且凋亡率随着计量的增加、时间的延长而逐渐增加。益肾固冲汤在40μg/ml量、作用72 h时具有统计学差异,细胞凋亡率最高,达17.93%,与正常对照组相比,G0/G1期细胞比率随作用时间延长在逐渐减少,G2/M期的细胞比率随作用时间延长在逐渐增加,细胞生长周期较明显停滞在G2/M期,具有明显时间依赖性。结论益肾固冲汤可以抑制人乳腺癌MCF-7细胞的增殖,诱导细胞凋亡,具有明显的量效和时效关系。细胞的增殖抑制与诱导凋亡作用与G2/M期有关。
Objective To investigate the effect of Yishen Guchong Decoction on inhibiting the proliferation and promoting apoptosis of breast cancer cells and the mechanism of anti-cancer molecules. Methods Human breast cell line (MCF) -7 cells were cultured in vitro. MTT assay was used to observe the inhibitory effect of YSKG on the proliferation of human breast cancer MCF-7 cells. Flow cytometry was used to detect the proliferation of human breast cancer Effect of MCF-7 on apoptosis and cell cycle. Results Yishen Guchong Decoction could inhibit the proliferation of human breast cancer cell line MCF-7, all of which had significant time-effect and dose-effect relationship. After treated with different concentrations of Yishen Guxue Decoction for 24, 48 and 72 h, the apoptosis of MCF-7 cells in various groups showed different degrees of apoptosis. With the increase of the measurement and the extension of time, gradually increase. Yishen Guchong Decoction had a statistical difference at the dose of 40 μg / ml for 72 h, with the highest rate of apoptosis (17.93%). Compared with the normal control group, the proportion of cells in G0 / G1 phase decreased gradually with the prolongation of action time , And the cell ratio of G2 / M phase increased gradually with the prolongation of acting time, and the cell growth cycle obviously stagnated in G2 / M phase with obvious time dependence. Conclusion Yishen Guchong Decoction can inhibit the proliferation of human breast cancer MCF-7 cells and induce apoptosis, with significant dose-effect and time-effect relationship. Cell proliferation inhibition and induction of apoptosis and G2 / M phase.