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辛伐他汀诱导K562 细胞凋亡过程中Caspase-3 、Caspase-9 活性变化

黄文芳, 杨永长, 刘 华, 陈 江, 周定安

黄文芳, 杨永长, 刘 华, 陈 江, 周定安. 辛伐他汀诱导K562 细胞凋亡过程中Caspase-3 、Caspase-9 活性变化[J]. 肿瘤防治研究, 2007, 34(01): 39-41. DOI: 10.3971/j.issn.1000-8578.1221
引用本文: 黄文芳, 杨永长, 刘 华, 陈 江, 周定安. 辛伐他汀诱导K562 细胞凋亡过程中Caspase-3 、Caspase-9 活性变化[J]. 肿瘤防治研究, 2007, 34(01): 39-41. DOI: 10.3971/j.issn.1000-8578.1221
HUANG Wen-fang, YANG Yong-chang, LIU Hua, CHEN Jiang, ZHOU Ding-an. Changes of Caspase-3 and Caspase-9 Activity during the Simvastatin-induced Apoptosis in K562 Cells[J]. Cancer Research on Prevention and Treatment, 2007, 34(01): 39-41. DOI: 10.3971/j.issn.1000-8578.1221
Citation: HUANG Wen-fang, YANG Yong-chang, LIU Hua, CHEN Jiang, ZHOU Ding-an. Changes of Caspase-3 and Caspase-9 Activity during the Simvastatin-induced Apoptosis in K562 Cells[J]. Cancer Research on Prevention and Treatment, 2007, 34(01): 39-41. DOI: 10.3971/j.issn.1000-8578.1221

辛伐他汀诱导K562 细胞凋亡过程中Caspase-3 、Caspase-9 活性变化

详细信息
  • 中图分类号: R733. 7

Changes of Caspase-3 and Caspase-9 Activity during the Simvastatin-induced Apoptosis in K562 Cells

  • 摘要: 目的 观察辛伐他汀诱导K562细胞凋亡过程中Caspase-3、Caspase-9活性的变化。方法 不同浓度辛伐他汀处理K562细胞,用细胞形态学、流式细胞技术检测细胞凋亡,比色法测定Caspase-3、Caspase-9活性。结果 5、10、20μmol/L辛伐他汀作用K562细胞48h后出现核固缩、核碎裂和凋亡小体等形态学改变,其凋亡率分别为(4.00±0.13)%、(6.24±0.18)%、(9.41±0.22)%,与对照组比较差异具有统计学意义(P〈0.01)。作用72h后细胞凋亡率分别为(7.62±0.21)%、(12.41±0.32)%、(19.08±0.26)%,与对照组比较差异具有统计学意义(P〈0.01)。同时Caspase-3、Caspase-9活性明显升高,10μmol/L与20μ/L组Caspase-3、Caspase-9活性与对照组比较差异具有统计学意义(P〈0.01)。结论 辛伐他汀可能通过活化Caspase-9,并进而活化Caspase-3诱导K562细胞凋亡。

     

    Abstract: Objective  To observe the variations of Caspase-3 and Caspase-9 activities in the process of simvastatin2induced apoptosis in K562 cells. Methods  K562 cells were exposed to different concent rations of simvastatin, cell morphological analysis and flow cytomet ry were performed to confirm cell apoptosis. Colorimet ric method was used to measure Caspase-3 and Caspase-9 activities. Results  K562 cells could be induced to undergo apoptosis af ter 5, 10, 20μmol/ L simvastatin t reatment for 48h, and the apoptotic rate was (4. 00 ±0. 13) %, (6. 24 ±0. 18) % and (9. 41 ±0. 22) % respectively, compared with the control group, it was significantly higher ( P < 0. 01) . At 72h, K562 cells were apoptotic with a rate of (7. 62 ±0. 21) %, (12. 41 ±0. 32) % and (19. 08 ±0. 26) % respectively, compared with the cont rol group, it was markedly higher ( P < 0. 01) . Furthermore, Caspase23 and Caspase29 activity in K562 cells elevated remarkably af ter 10, 20μmol/ L simvastatin t reatment for 48h and 72h, compared with the cont rol group, it was markedly higher ( P < 0. 01) . Conclusion  K562 cells can be induced to undergo apoptosis by simvastatin, the underlying mechanism might be related to upregulation of Caspase-9 activity which subsequently t ransforms Caspase-3 into it s active form.

     

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出版历程
  • 收稿日期:  2005-12-04
  • 修回日期:  2006-04-05
  • 刊出日期:  2007-01-04

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