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目的探讨硒-甲基硒代半胱氨酸(MSC)对人乳腺癌MDA-MB-231细胞的生长抑制作用。方法不同浓度MSC培养液(12.5、25.0、50.0、100.0、200.0μmol/L)作用于MDA-MB-231细胞24、48 h,噻唑蓝法检测M SC对细胞增殖的抑制作用;Hoechst染色法观察细胞凋亡形态;试剂盒检测超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-Px)活力变化。结果 MSC对细胞增殖具有抑制作用,与对照组比较(100±0.00%),200μmol/L M SC处理24、48 h细胞生存率[分别为(64.15±2.81)%、(42.57±2.25)%]明显下降(P<0.01),呈剂量和时间效应关系;Hoechst染色结果显示,高剂量M SC组细胞可见明显染色质凝聚现象;与对照组[SOD(82.47±1.99)、GSH-Px(46.69±0.55)U/mgprot、MDA(5.80±0.11)μmol/mgprot]比较,200μmol/L MSC处理组细胞24 h时,细胞内SOD、GSH-Px活力[分别为(20.99±3.03)、(22.00±0.75)U/mgprot]明显下降,MDA含量[(36.20±0.25)μmol/mgprot]明显升高,差异有统计学意义(P<0.01);相同剂量MSC作用MDA-MB-231细胞48 h时,细胞内氧化应激指标变化趋势与作用24 h时趋势相同。结论 MSC能够抑制乳腺癌细胞MDAM B-231的增殖,诱导其凋亡,其机制可能与细胞内氧化应激状态改变有关。
Objective To investigate the inhibitory effect of selenium-methylselenocysteine (MSC) on the growth of human breast cancer MDA-MB-231 cells. Methods MDA-MB-231 cells were treated with various concentrations of MSC (12.5, 25.0, 50.0, 100.0 and 200.0 μmol / L) for 24,48 h. MTT assay was used to detect the inhibitory effect of M SC on cell proliferation. Hoechst staining The morphological changes of apoptotic cells were detected by enzyme-linked immunosorbent assay (ELISA). The activity of superoxide dismutase (SOD), malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) Results MSC had inhibitory effect on cell proliferation. Compared with the control group (100 ± 0.00%), MSC survival at 24 h and 48 h after treatment with 200 μmol / LM SC [(64.15 ± 2.81)% and (42.57 ± 2.25)%] (P <0.01). The results of Hoechst staining showed that chromatin condensation was observed in high-dose M SC cells. Compared with the control group [SOD (82.47 ± 1.99), GSH-Px The activities of SOD and GSH-Px in cells treated with 200μmol / L MSC for 24 h were (20.99 ± 3.03) and (22.00 ± 0.75) mg / MDA content [(36.20 ± 0.25) μmol / mgprot] was significantly increased in the MDA-MB-231 cells treated with the same dose of MS for 48 h (P <0.01) The trend of oxidative stress indicators and the role of the same trend at 24 h. Conclusion MSC can inhibit the proliferation and induce the apoptosis of MDAM B-231 breast cancer cells, which may be related to the change of intracellular oxidative stress.