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目的:探讨拓朴替康诱导K562细胞凋亡的相关信号转导途径。方法:0.1μmol/L的拓朴替康处理K562细胞24h时,通过流式细胞仪(FCM)和片段DNA含量检测研究拓朴替康对靶细胞的促凋亡活性;采用免疫印迹法和γ-32P掺入法测定拓朴替康对p38MAPK含量及其活性的影响。结果:FCM检测发现在K562细胞周期图中出现一凋亡峰,凋亡细胞比率为16.9%,凋亡细胞特有的片段DNA含量为(45.9±1.0)%;p38MAPK含量及其活性明显升高,分别为对照组的4.9倍和4.1倍。结论:拓朴替康诱导K562细胞凋亡可能通过激活p38MAPK来实现。
Objective: To investigate the signal transduction pathways involved in topotecan-induced apoptosis in K562 cells. Methods: The apoptosis of K562 cells was detected by flow cytometry (FCM) and DNA fragment content at the concentration of 0.1μmol / L Topotecan for 24 h. The apoptosis of target cells was detected by Western blot and γ Effect of topotecan on p38MAPK content and its activity by -32P incorporation method. Results: FCM showed a apoptotic peak in K562 cell cycle. The percentage of apoptotic cells was 16.9% and that of apoptotic cells was (45.9 ± 1.0)%. The content of p38MAPK and its activity were significantly increased, Respectively, 4.9 times and 4.1 times the control group. Conclusion: Topotecan can induce the apoptosis of K562 cells by activating p38MAPK.