摘要
目的 :观察粒细胞集落刺激因子 (G -CSF)对阿糖胞苷 (Ara -C)诱导HL - 6 0白血病细胞凋亡的调控作用。方法 :应用细胞培养技术、细胞凋亡形态、二苯胺法DNA片段化定量和MTT法来观察HL - 6 0白血病细胞的增殖、凋亡和细胞药敏的变化。结果 :G -CSF有刺激HL - 6 0白血病细胞的增殖的作用 ,其细胞集落为76 5± 18 0 ,而对照组仅为 46 5± 13 5 (P <0 0 1,n =5 )。Ara -C (10mg/L)作用于HL - 6 0白血病细胞 4h ,DNA片段率为 32 3%± 6 5 % ,同时加入G -CSF和Ara -C作用于HL - 6 0白血病细胞 4h ;DNA片段率为 2 3 6 %±7 2 % ,两组比较有非常显著性差异 (P <0 0 1)。HL - 6 0白血病细胞加入G -CSF后对Ara -C的IC5 0 (18 85±3 2 1)可看出比单用Ara -C(15 2 9± 2 47)的敏感性低 (P <0 0 5 )。结论 :G -CSF能刺激HL - 6 0白血病细胞增殖 ;抑制Ara -C诱导HL - 6 0白血病细胞的凋亡 ;能降低HL - 6 0白血病细胞对Ara
AIM: To investigate the effect of granulocyte colony stimulating factor (G-CSF) on arabinosyl cytosine (Ara-C)-induced apoptosis in HL-60 leukemia cells. METHODS: The proliferation of HL-60 leukemia cell was observed by hemopoietic cell culture. Apoptosis was measured by the morphology of apoptosis cell , the quantitation of DNA fragmentation with the diphenylamine reaction. The change in drug sensitivity was measured by “MTT”. RESULTS: G-CSF could stimulate the proliferation of HL-60 leukemia cell and colonies of cell increased to 76.5±18.0, compared to the control group (46.5±13.5. P<0.01. n=5).When the cells were incubated with Ara-C (10 mg/L) for 4 h, the percentage of DNA fragmentation 32.3%±6.5% was higher than that of the G-CSF and Ara-C group 23.6%±7.2% (P<0.01). It showed that G-CSF could suppress the apoptosis of HL-60 leukemia cell induced by Ara-C. When the cells were treated with G-CSF,IC50 of the cell to Ara-C (18.85±3.21) was higher than that treated only with Ara-C(15.29±2.47)(P<0.05). CONCLUSION: G-CSF could stimulate the proliferation of the HL-60 leukemia cell, suppress the apoptosis of the cell induced by Ara-C, and reduce the sensitivity of HL-60 leukemia cell to Ara-C.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2000年第11期1207-1209,共3页
Chinese Journal of Pathophysiology
