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为了观察组蛋白去乙酰化酶抑制剂丙戊酸(VPA)、曲古抑菌素(TSA)对K562细胞和HL60细胞的抗肿瘤作用以及它们同全反式维甲酸(ATRA)之间的协同效应,采用绘制细胞生长曲线,计算半数抑制浓度(IC50)以及集落抑制试验等方法观察VPA,TSA以及全反式维甲酸(ATRA)在不同浓度或不同组合条件下对HL60细胞和K562细胞的增殖抑制作用。采用细胞化学染色、分化抗原检测、细胞周期测定、联合NBT与MTT还原试验计算A(NBT)/A(MTT)值等方法分析细胞的分化或凋亡特点。结果显示,在体外培养体系中,VPA对HL60细胞的IC50值低于对K562细胞的IC50值。ATRA能明显增强VPA、TSA对HL60细胞以及VPA对K562细胞集落形成的抑制。HL60经VPA处理后出现粒系表型,NBT还原率增加,CD11b表达增强,而K562细胞未显示分化迹象。结论:VPA和TSA抑制HL60细胞增殖,VPA诱导HL60细胞向粒系分化,这些作用均能被ATRA增强;VPA和TSA对K562细胞增殖抑制作用较弱,不能诱导K562细胞分化。
To observe the antitumor effects of histone deacetylase inhibitors valproic acid (VPA), trichostatin (TSA) on K562 cells and HL60 cells and their synergy with all-trans retinoic acid (ATRA) The cell growth curve, IC50 and colony inhibition test were used to observe the proliferation of HL60 cells and K562 cells under different concentrations or different combinations of VPA, TSA and all-trans retinoic acid (ATRA) Inhibition. The characteristics of cell differentiation or apoptosis were analyzed by cytochemical staining, differentiation antigen test, cell cycle assay, NBT / MTT assay and NBT / MTT assay. The results showed that the IC50 of VPA in HL60 cells was lower than that of K562 cells in in vitro culture system. ATRA can significantly enhance VPA, TSA on HL60 cells and VPA K562 cell colony formation inhibition. After HL60 treated with VPA, the phenotype of myeloid appeared, the NBT reduction rate increased, CD11b expression increased, while K562 cells did not show signs of differentiation. CONCLUSION: VPA and TSA can inhibit the proliferation of HL60 cells and VPA can induce the differentiation of HL60 cells into granulocytes. All of these effects can be enhanced by ATRA. VPA and TSA can not inhibit the proliferation of K562 cells and can not induce the differentiation of K562 cells.