| 蔡心颖,林东麒,陈 清,杨 虹,郭江睿,李 暐.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[J].,2020,(4):648-653 |
| 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 |
| The Inhibitory Effect of Flubenazole on Proliferation of Human Acute Myeloid Leukemia HL-60 Cells |
| 投稿时间：2019-06-30 修订日期：2019-07-26 |
| DOI：10.13241/j.cnki.pmb.2020.04.010 |
| 中文关键词: 氟苯达唑 急性髓系白血病 周期 凋亡 |
| 英文关键词: Flubendazole Acute myeloid leukemia Cell Cycle Apoptosis |
| 基金项目:福建省自然科学基金项目（2017J01531）；福建省卫生健康中青年骨干人才培养项目（2018-ZQN-33）；福建省青年科技人才创新项目（2017J05127） |
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| 中文摘要: |
| 摘要 目的：研究氟苯达唑对人急性髓系白血病HL-60细胞增殖的抑制作用，明确氟苯达唑对HL-60细胞周期，凋亡发生的作用机制。方法：噻唑蓝法（MTT）检测氟苯达唑对人急性髓系白血病HL-60细胞的生长抑制作用，流式细胞术检测氟苯达唑对HL-60细胞周期，DNA片段化的影响，免疫印迹法检测Caspase, Raf, Bcl-2家族蛋白表达。结果：氟苯达唑抑制人急性髓系白血病HL-60细胞生长， HL-60细胞G2/M期增加，与阴性对照组相比，在一定的剂量和时间内，差别具有显著统计学意义；DNA片段化上升，0.25,0.5,1 μM组与对照组相比差别具有显著统计学意义，促使Cleaved PARP，Cleaved-caspase 3，Cleaved-caspase 9蛋白表达量趋势增加；Bag-1和Bcl-2蛋白表达量降低；b-raf，c-raf磷酸化蛋白表达水平逐渐降低。结论：氟苯达唑通过诱导HL-60细胞阻滞于G2/M期，增加DNA片段化水平，激活Caspase, Raf, Bcl-2家族介导的凋亡相关通路抑制人急性髓系白血病HL-60细胞增殖，诱导人急性髓系白血病HL-60细胞发生凋亡而发挥抗肿瘤作用。 |
| 英文摘要: |
| ABSTRACT 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 tetrazolium(MTT) assay was used to evaluatethe growth inhibition effects of flubendazole on human acute myeloid leukemia HL-60 cells. Flow cytometry was used to detect the effect of flubendazole on HL-60 cell cycle and DNA fragmentation. Western blotting was used to detect the expression of Caspase, Raf, and Bcl-2 family 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. |
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