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半夏总生物碱对人肝癌细胞增殖的抑制作用研究

     

摘要

目的:探讨半夏总生物碱( TATP)对人肝癌细胞株QJY-7703增殖的影响。方法采用四甲基偶氮唑盐( MTT)比色法及集落形成率实验,检测不同浓度的TATP对QJY-7703细胞株的生长抑制作用;应用单细胞凝胶电泳技术检测TATP导致QJY-7703细胞的DNA损伤情况。结果人肝癌细胞QJY-7703经TATP处理后,其体外增殖能力明显下降,且与药物的剂量、加药时间呈正相关,与对照组比较,差异均有统计学意义(24 h:对照组QJY-7703细胞增殖OD490=0.486±0.037,TATP组2.5、10.0、30.0、50.0 mg/L时的OD490分别为0.475±0.026、0.377±0.029、0.286±0.026、0.242±0.023;48 h:对照组OD490=0.793±0.046,TATP组2.5、10.0、30.0、50.0 mg/L时的OD490分别为0.747±0.028、0.497±0.025、0.287±0.021、0.207±0.020)(P<0.01或P<0.05)。单细胞凝胶电泳(SCGE)中,TATP组细胞尾DNA含量:对照组为(6.92±4.85)mg/L,TATP组10.0、40.0 mg/L时分别为(17.30±5.39)mg/L、(36.52±8.67)mg/L;尾长:对照组为(16.06±9.17)μm,TATP组10.0、40.0 mg/L时分别为(29.29±13.09)μm、(65.33±17.06)μm;尾动量:对照组为(0.97±0.34)μm,TATP组10.0、40.0 mg/L时分别为(7.87±4.04)μm、(21.43±7.67)μm,与对照组相比差异有统计学意义(P<0.01),且呈现浓度依赖性。结论在体外培养的条件下,一定剂量的TATP能明显抑制QJY-7703细胞增殖,其机制可能与DNA的损伤作用有关。%Objective To investigate the inhibitive effect of total alkaloids from Pinellia ternate ( TAPT) on the proliferation of human hepatic carcinoma strain QJY-7703.Methods The proliferation inhibition of human hepatic carcinoma cells treated with TAPT was measured with methyl thiazolil tetracolium colorimetic (MTT) method and plate clone formation assay to detect the inhibitive effect of different concentrations of TAPT on the growth of QJY-7703 strains.Single cell gel electrophoresis (SCGE) was used to detect QJY-7703 cell DNA damage induced by TAPT .Results When compared with the control group , in vitro proliferation of QJY-7703 cells treated with TAPT was decreased significantly , and it was positively correlated with drug dosage and medication time , and statistical sig-nificance could be seen, when comparisons were made (P<0.01,P<0.05).In SCGE detection, significant differences could be seen in cell tail DNA content , tail length and tail movement in the TAPT experimental group , when compared with those of the control group (P<0.01), and a dose-dependent relationship was quite marked .Conclusion In vitro, a certain dosage of TAPT could obviously in-hibit the proliferation of QJY-7703 cells, the mechanism of which might be correlated to DNA damage induced by TAPT .

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