摘要
目的 :为探讨Wortmannin抑制磷酰肌醇 - 3激酶 (PI- 3K)途径对K5 62 ,NB4细胞增殖的影响 ,探寻慢性髓细胞性白血病 (CML)的治疗新途径 .方法 :用磷酰肌醇 - 3激酶 (PI - 3K)特异抑制剂Wort mannin抑制PI - 3K活性 ,观察慢性髓细胞性白血病细胞系K5 62细胞和急性早幼粒细胞性白血病细胞系NB4细胞在 2 4,48,72h增殖能力的变化 .t检验统计分析 .结果 :K5 62和NB4细胞在 2 4,48,72h的增殖抑制率分别为 3 4 67% ,5 7 46% ,65 85 %和 2 6 2 9% ,5 5 1% ,2 10 % .集落形成实验以GM -CSF为主要生长刺激物的培养体系在 3 7℃ ,5 %CO2 孵箱培养 14d后细胞系的集落数和集落形成率分别为K5 62 :80 75±10 2 4和 16 15 % ,K5 62 +WT :3 8 0 0± 12 75和 7 60 % ,NB4:2 9 5 0± 5 97和 5 90 % ,NB4+WT :3 0 5 0± 5 74和 6 10 % .集落形成抑制率为 :5 2 94%和 3 3 9% .结论 :Wortmannin可显著抑制K5 62细胞的增殖和集落形成 ,而对NB4细胞无明显影响 (P均 <0 0 5 ) .Wortmannin可以通过抑制PI - 3K通路抑制K5 62细胞的增殖 。
To explore the effects of wortmannin inhibiting phosphatidylinositol-3 kinase's approach on K562 and NB4 cell proliferation and try to find out a new approach treating chronic myelogenous leukemia. Using wortmannin to restrain the PI-3K vitality in 0.25?μmol/L consistency and observing their effects on K562 cells and NB4 cells. The results showed that the growth inhibition rates of K562 cells were 41.33%,57.46%,65.85% respectively, NB4 cells were 26.29%, 5.51%, 2.10% respectively in 24?hours,48?hours,72?hours; that K562 and NB4 cells colony formation rates were 16.15% ,7.60%,5.90%,6.10% and colony formation inhibition rates were 52.94% and 3.39% . Wortmannin can inhibit K562 cells proliferation, but had no effect on NB4 cells proliferation. Conclusion: Wortmannin can inhibit the K562 cells proliferation by suppressing PI3K activity.
出处
《昆明医学院学报》
2003年第2期36-38,共3页
Journal of Kunming Medical College
基金
云南省自然科学基金资助项目 ( 2 0 0 0C0 0 3 0Q)
