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为了探讨丙戊酸(valproic acid,VPA)对白血病HL-60细胞诱导凋亡的作用及其可能的机制,采用细胞毒性试验(CCK-8法)观察不同浓度VPA在不同作用时间对HL-60细胞增殖的影响,采用荧光显微镜检及流式细胞术检测细胞凋亡,并观察VPA作用后HL-60细胞端粒酶亚单位h-tert基因、凋亡相关蛋白表达和caspase-3活性的变化。结果表明:VPA呈剂量依赖性抑制HL-60细胞增殖(r=-0.87).,诱导细胞凋亡;同时,抗凋亡蛋白BCL-2表达明显下降,促凋亡蛋白BAX表达上调,caspase-3活性增强,h-tert mRNA表达逐渐下降,HL-60细胞的凋亡率与h-tert mRNA表达呈负相关。结论:VPA可抑制白血病HL-60细胞增殖,诱导细胞凋亡;VPA可能通过下调h-tert mRNA、BCL-2蛋白表达,上调BAX表达及增强caspase-3活性而发挥抗白血病作用。
To investigate the effect of valproic acid (VPA) on the apoptosis of HL-60 leukemia cells and its possible mechanism, the cytotoxicity assay (CCK-8 method) was used to observe the effects of different concentrations of VPA on HL-60 Cell proliferation. Fluorescence microscopy and flow cytometry were used to detect apoptosis. The changes of h-tert gene, apoptosis-related protein and caspase-3 activity in HL-60 cells after VPA treatment were observed . The results showed that: VPA inhibited the proliferation of HL-60 cells in a dose-dependent manner (r = -0.87), and induced the apoptosis of cells; at the same time, the expression of anti-apoptotic protein BCL- 3 activity, the h-tert mRNA expression gradually decreased, and the apoptosis rate of HL-60 cells was negatively correlated with the expression of h-tert mRNA. VPA could inhibit leukemia HL-60 cells proliferation and induce apoptosis. VPA may play an anti-leukemia role by down-regulating h-tert mRNA and BCL-2 protein expression, up-regulating BAX expression and enhancing caspase-3 activity.