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袁国海, 黄秋, 邵继红, 罗雅婕, 谢蒙蒙. 硒-甲基硒代半胱氨酸诱导乳腺癌细胞凋亡作用[J]. 中国公共卫生, 2016, 32(9): 1183-1185. DOI: 10.11847/zgggws2016-32-09-13
引用本文: 袁国海, 黄秋, 邵继红, 罗雅婕, 谢蒙蒙. 硒-甲基硒代半胱氨酸诱导乳腺癌细胞凋亡作用[J]. 中国公共卫生, 2016, 32(9): 1183-1185. DOI: 10.11847/zgggws2016-32-09-13
YUAN Guo-hai, HUANG Qiu, SHAO Ji-hong.et al, . Inhibitory effect of Se-methylselenocysteine on human breast cancer cells[J]. Chinese Journal of Public Health, 2016, 32(9): 1183-1185. DOI: 10.11847/zgggws2016-32-09-13
Citation: YUAN Guo-hai, HUANG Qiu, SHAO Ji-hong.et al, . Inhibitory effect of Se-methylselenocysteine on human breast cancer cells[J]. Chinese Journal of Public Health, 2016, 32(9): 1183-1185. DOI: 10.11847/zgggws2016-32-09-13

硒-甲基硒代半胱氨酸诱导乳腺癌细胞凋亡作用

Inhibitory effect of Se-methylselenocysteine on human breast cancer cells

  • 摘要: 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、200.0 μmol/L)作用于MDA-MB-231细胞24、48 h,噻唑蓝法检测MSC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%),200 μmol/L MSC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MSC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, 200 μmol/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MDA-MB-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。

     

    Abstract: Objective To observe restrictive impact of Se-methylselenocysteine (MSC) on the growth of human breast cancer cells (MDA-MB-231).Methods MDA-MB-231 cells were challenged with different concentrations of MSC (12.5,25,50,100,and 200 μmol/L)for 24 and 48 hours,respectively.The inhibition rate of MDA-MB-231 cells was assayed with 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyltetrazolium bromide (MTT) assay.The cell apoptosis was observed with Hoechst stain.The activities of superoxide dismutase (SOD),malondialdehyde (MDA)and glutathione peroxidase (GSH-Px) in MDA-MB-231 cells were determined with test kit.Results MSC can inhibit proliferation of MDA-MB-231 cells.Compared with that of control group(100±0.00%),the survival rate of MDA-MB-231 cells treated with 200 μmol/L MSC decreased remarkably at 24 (64.15±2.81%)and 48 hours (42.57±2.25%).MTT assay showed that MSC could inhibit the proliferation of MDA-MB-231 cells in dose- and time-dependent manner (P<0.01).Hoechst stain demonstrated that there were obvious chromatin condensations in MDA-MB-231 cells of MSC pretreatment group.Compared with those in the control group,the activities of SOD (20.99±3.03 vs.82.47±1.99 U/mg protein) and GSH-Px (22.00±0.75 vs.46.69±0.55 U/mg protein)declined but the activity of MDA (36.20±0.25 vs.5.80±0.11 μmol/mg protein)increased obviously in the MDA-MB-231 cells treated with 200 μmol/L MSC for 24 hours and the variations were also observed in the cells with the same MSC treatment for 48 hours.Conclusion MSC can inhibit proliferation and induce apoptosis in human breast cancer cell line MDA-MB-231 in dose- and time-dependent manner;the mechanism of the inhibitive effect of MSC may related to the change in antioxidant activity.

     

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