拓朴替康诱导K562细胞凋亡时p38MAPK的变化  

The change of p38MAPK in the apoptosis of K562 cells induced by topotecan

作　　者：尚振川[1] 孙浩平[1] 赵越华[1] 邓涛[1] 范方毅[1] 李翼[1] 

机构地区：[1]成都军区总医院血液内科,610083

出　　处：《实用医学杂志》2006年第11期1225-1227,共3页The Journal of Practical Medicine

基　　金：国家自然科学基金课题资助项目(编号:39670330;39770336)

摘　　要：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 study the signal transduction in apoptosis of K562 cells induced by topotecan. Methods After K562 cells were treated by topotecan in 24 hours, the apoptosis effect was evaluated by FCM and DNA fragment. p38MAPK content was detected by Western blot and p38MAPK activity was assayed by the measurement of the incorporation of ^32P from [γ^32P] ATP into peptide substrates. Results An apoptosis peak was found in the K562 cell cycle by FCM and the apoptosis rate was 16.9%. The content of DNA fragment was （45.9 ± 1.0）%. p38MAPK content was 4. 9 times and p38MAPK activity was 4. 1 times higher than that in the control group, respectively （ P〈0.05）. Conclusion Topotecan could induce apoptosis of K562 cells by activating p38MAPK.

关 键 词：K562细胞 托泊替坎 P38丝裂原活化蛋白激酶类 细胞凋亡 

分 类 号：R730.5[医药卫生—肿瘤]