当前位置:主页 > 医学论文 > 肿瘤论文 >

芬苯达唑对慢性髓系白血病K562细胞的增殖抑制作用

发布时间:2018-03-19 07:05

  本文选题:芬苯达唑 切入点:慢性髓系白血病 出处:《中国病理生理杂志》2017年06期  论文类型:期刊论文


【摘要】:目的:探讨抗寄生虫药芬苯达唑对慢性髓系白血病细胞K562的作用及机制。方法:采用CCK-8法检测芬苯达唑对K562和正常人外周血单个核细胞(PBMC)生长的影响;台盼蓝拒染实验检测芬苯达唑对K562细胞活力的影响;瑞氏染色观察芬苯达唑对K562细胞形态的影响;流式细胞术检测芬苯达唑对K562细胞周期分布的影响;Western blot检测芬苯达唑对K562细胞周期相关蛋白表达的影响;免疫荧光观察芬苯达唑对K562细胞核的改变。结果:芬苯达唑能够显著抑制K562细胞的生长,而对PBMC生长无明显影响;进一步的研究发现,芬苯达唑显著抑制K562细胞增殖并诱导细胞发生G_2/M期阻滞;芬苯达唑处理K562细胞后,细胞分裂周期蛋白25C(Cdc25C)磷酸化、周期素依赖性激酶1(Cdk1)-Tyr15去磷酸化以及cyclin B1磷酸化增加;免疫荧光结果证实芬苯达唑诱导K562多核细胞增多(P0.01),发生有丝分裂灾难。结论:芬苯达唑通过调控周期相关蛋白诱导K562细胞发生G_2/M期阻滞。
[Abstract]:Objective: to investigate the effect and mechanism of fenbendazole on the growth of K562 cells. Methods: the effects of fenbendazole on the growth of K562 and normal peripheral blood mononuclear cells (PBMCs) were detected by CCK-8 assay. The effect of fenbendazole on the viability of K562 cells was detected by trypan blue exclusion assay, and the effect of fenbendazole on the morphology of K562 cells was observed by Rayleigh staining. The effect of fenbendazole on cell cycle distribution of K562 cells was detected by flow cytometry. The effect of fenbendazole on the expression of cell cycle related proteins in K562 cells was detected by Western blot. Results: fenbendazole could significantly inhibit the growth of K562 cells, but had no effect on the growth of PBMC. Fenbendazole significantly inhibited K562 cell proliferation and induced GV / M arrest, and after treatment with fenbendazole, cell mitotic cyclin 25 cdc25C) phosphorylation, cyclin dependent kinase 1 (CDK 1) -Tyr15 dephosphorylation and cyclin B1 phosphorylation increased. The results of immunofluorescence showed that fenbendazole induced K562 cells to increase P0.01G and induce mitotic disaster. Conclusion: Fenbendazole induces G 2 / M arrest of K562 cells by regulating cycle related proteins.
【作者单位】: 温州医科大学检生学院;
【基金】:国家自然科学基金资助项目(No.81400125;No.81372826) 教育部博士点新教师类资助项目(No.20133321120003) 浙江省自然科学基金资助项目(No.LQ13H080002)
【分类号】:R733.72


本文编号:1633316

资料下载
论文发表

本文链接:https://www.wllwen.com/yixuelunwen/zlx/1633316.html


Copyright(c)文论论文网All Rights Reserved | 网站地图 |

版权申明:资料由用户c4ee5***提供,本站仅收录摘要或目录,作者需要删除请E-mail邮箱bigeng88@qq.com