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作 者:刘复强[1] 靳新强[1] 杨敏[1] 杨凌[1] 王津津[1] 吴轶苹[1] 翟艳苓[1] 刘元波[1]
机构地区:[1]首都医科大学附属北京同仁医院,北京100730
出 处:《中国实验血液学杂志》2000年第4期275-279,共5页Journal of Experimental Hematology
摘 要:为探讨rhGM CSF对VP 16诱导的HL 60细胞凋亡的影响 ,我们观察了预先应用rhGM CSF孵育的HL 60细胞由VP 16诱导的凋亡过程及凋亡相关基因bcl 2和fas的表达变化。应用光学显微镜和电子显微镜观察细胞形态和超微结构的变化 ,凝胶电泳检测DNA的碎片 ,流式细胞术检测细胞凋亡率、bcl 2和fas的表达。实验结果显示 ,rhGM CSF可抑制VP 16诱导的HL 60细胞的凋亡 ,它加强了VP 16对bcl 2表达的下调作用 ,抑制了VP 16对fas表达的上调作用。由此推测 ,rhGM CSF可能是通过下调fas表达降低HL 60细胞对VPIn order to investigate the effects of rhGM-CSF on apoptosis of HL-60 cells induced with VP-16 treatment, HL-60 cells were first incubated with rhGM-CSF before they were treated with VP-16. The apoptosis processes and the changes in apoptosis related gene bcl-2 and fas expression were observed. The morphological and ultrastructural changes were observed under optics microscope and electromicroscope. DNA fragmentation were detected by agarose gel electrophoresis, the apoptotic rate, bcl-2 and fas expression with flow cytometry. Our results showed that rhGM-CSF inhibited the apoptosis of HL-60 cells induced with VP-16 treatment, which enhanced the down-regulation of bcl-2 expression, but inhibited the up-regulation of fas expression. So it suggested that rhGM-CSF can decrease the sensitivity of HL-60 cells to VP-16, probably by down-regulation of fas expression.
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