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目的:探讨曲古抑菌素A(TSA)在体外诱导急性早幼粒白血病HL-60细胞凋亡的机制。方法:采用MTT方法检测TSA对HL-60细胞增殖的影响,流式细胞术检测细胞周期和细胞凋亡,RT-PCR检测凋亡相关基因Bax、Caspase-9和Caspase-3的表达。结果:0.1μmol/L的TSA可明显抑制细胞增殖,P<0.01;0.05μmol/L的TSA可使细胞周期阻滞在G0/G1期(P<0.05),但0.1μmol/L的TSA才能引起细胞凋亡(P<0.01);经0.1μmol/L的TSA作用12 h后,Bax、Caspase-9和Caspase-3基因表达明显升高,P<0.01。结论:TSA诱导HL-60细胞凋亡的机制在于引起细胞周期阻滞,上调Bax、Caspase-9和Caspase-3的表达。
Objective: To investigate the mechanism of trichostatin A (TSA) inducing apoptosis in acute promyelocytic leukemia HL-60 cells in vitro. Methods: The effect of TSA on the proliferation of HL-60 cells was detected by MTT assay. The cell cycle and apoptosis were detected by flow cytometry. The expression of apoptosis-related genes Bax, Caspase-9 and Caspase-3 were detected by RT-PCR. Results: TSA at a concentration of 0.1μmol / L significantly inhibited cell proliferation, P <0.01; TSA at a concentration of 0.05μmol / L blocked cell cycle arrest at G0 / G1 phase (P <0.05) (P <0.01). The expressions of Bax, Caspase-9 and Caspase-3 were significantly increased after treated with 0.1μmol / L TSA for 12 h (P <0.01). CONCLUSIONS: The mechanism of TSA-induced HL-60 cell apoptosis is that it causes cell cycle arrest and up-regulates the expression of Bax, Caspase-9 and Caspase-3.