氟苯达唑对人急性髓系白血病 HL-60 细胞的增殖抑制作用研究.

Objective: To investigate the inhibitory effect of flubendazole on the proliferation of human acute myeloid leukemia HL-60 cells, and clarifying the mechanism of flubendazole on cell cycle and apoptosis of HL-60 cells . Methods: Methyl thiazolyl tetra-zolimn (MTT) assay was used to evaluatethe growth inhibition effects of flubendazole on hmnan acute myeloid leukemia HL-60 cells. Flow cytometry was used to detect the effect of flubendazole on HL-60 cell cycle and DNA frag mentation. Western blotting was used to detect the expression of Caspase, Raf, and Bcl-2 furnily proteins. Results: Flubendazole inhibited the growth of human acute myeloid leukemia HL-60 cells. The G2/M phase, the DNA fragmentation and the expression of Cleaved PARP, Cleaved-caspase 3, and Cleaved-caspase 9 of HL-60 cells increased. The expression of Bag-1 protein was decreased and the Bcl-2 was increased. The b-raf and the c-raf phosphorylation protein levels was inhibited by Flubendazole. Conclusion: The G2/M phase of human acute myeloid leukemia HL-60 cells was arrested by flubendazole, and increasing DNA fragmentation level and activating Caspase, Raf and Bcl-2 family apoptosis-related pathways which Inducing apoptosis in human acute myeloid leukemia HL-60 cells and taking anti-tumor effects. [ABSTRACT FROM AUTHOR]