• 藤黄酸调控白血病K562细胞GFI-1表达及对细胞增殖和凋亡的影响
  • Gambogic acid regulates GFI-1 expression in K562 cells and its effects on cell proliferation and apoptosis
  • 刘晓倩.藤黄酸调控白血病K562细胞GFI-1表达及对细胞增殖和凋亡的影响[J].内科急危重症杂志,2021,27(1):54-57
    DOI:10.11768/nkjwzzzz20210115
    中文关键词:  藤黄酸  K562细胞  细胞增殖  细胞凋亡  蛋白酶体通道  独立生长因子
    英文关键词:
    基金项目:武汉市卫生计生委医学科研项目(No:WX18C32);湖北省卫生健康委联合基金项目(No:WJ2018H0113)
    作者单位E-mail
    刘晓倩 武汉科技大学医学院 cwei200408@163.com 
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    中文摘要:
          目的: 探讨藤黄酸对白血病K562细胞增殖和凋亡的影响及可能的机制。方法:体外培养K562细胞,采用CCK-8法检测不同浓度藤黄酸(0、0.2、0.4、0.8、1.2、2.0μmol/L)处理24、48、72h后K562细胞增殖率;用流式细胞术检测K562细胞的凋亡和周期;采用实时荧光定量聚合酶链反应(RT-qPCR))和Western blot法检测独立生长因子1(GFI-1) 的mRNA及蛋白表达水平。结果: 藤黄酸可以抑制K562细胞的增殖,并呈剂量、时间依赖性;0.4μmol/L藤黄酸处理24h后的K562细胞凋亡率增加;藤黄酸对GFI-1的mRNA表达无显著影响,藤黄酸可以下调GFI-1蛋白的表达;藤黄酸及蛋白酶体抑制剂(MG132)共处理后的K562细胞GFI-1蛋白水平较藤黄酸组升高;藤黄酸及氯喹(CQ)共处理后的K562细胞GFI-1蛋白水平与藤黄酸组无统计学差异(P>0.05)。结论: 藤黄酸可以有效抑制K562细胞的增殖并诱导细胞凋亡;藤黄酸可以诱导K562细胞G0/G1期及S期阻滞;藤黄酸通过蛋白酶体途径促进GFI-1蛋白降解。
    英文摘要:
          Objective: To investigate the effect of gambogic acid on proliferation and apoptosis of leukemic K562 cells and its possible mechanism. Methods: K562 cells were cultured in vitro, and the proliferation rate of K562 cells after treatment with different concentrations of gambogic acid (0, 0.2, 0.4, 0.8, 1.2, 2.0 μmol/L) for 24, 48, and 72h was determined by CCK-8 method. Flow cytometry was used to detect the apoptosis and cycle death of K562 cells. K562 cells were treated by different methods, and mRNA and protein expression levels of independent growth factor 1 (GFI-1) were detected by real-time fluorescence quantitative polymerase chain reaction (RT-qPCR) and Western blotting respectively. Results The proliferation of K562 cells was inhibited by gambogic acid in a dose-dependent and time-dependent manner. After treatment with 0.4μmol/L gambogic acid for 24h, the apoptosis rate of K562 cells increased. The GFI-1 mRNA expression was not significantly affected by gambogic acid, but the GFI-1 protein expression was down-regulated by gambogic acid. GFI-1 protein level in K562 cells treated with gambogic acid + proteasome inhibitor was increased as compared with that in the gambogic acid group, and GFI-1 protein level in K562 cells treated with gambogic acid + chloroquine showed no significantly different from that in the gambogic acid group. Conclusion: Gambogic acid can effectively inhibit the proliferation of K562 cells and induce cell apoptosis; Gambogic acid can induce arrest of K562 cells at G0/G1 phase and S phase; Gambogic acid promotes the degradation of GFI-1 protein by the proteasome pathway.