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目的研究硒化壳聚糖对耐阿霉素慢性粒细胞白血病细胞株K562/ADM增殖的影响,探讨这种影响与PI-3K/Akt信号途径的关系。方法硒化壳聚糖作用K562/ADM细胞后,应用MTT法和克隆形成法检测硒化壳聚糖对细胞增殖和存活的影响,计算逆转倍数;应用免疫印迹法检测p-Akt蛋白表达的改变。结果随着硒化壳聚糖浓度的增加,细胞增殖抑制率相应增加,存活率相应减少,呈剂量时间效应关系。硒化壳聚糖能够下调p-Akt表达(P<0.01),明显增强ADM对K562/ADM细胞的增殖抑制作用(P<0.05,P<0.01),对细胞耐药产生一定的逆转作用。结论硒化壳聚糖可通过抑制PI-3K/Akt信号途径对耐药白血病细胞株K562/ADM产生增殖抑制和多药耐药逆转作用。
Objective To study the effect of selenized chitosan on the proliferation of adriamycin-resistant chronic myeloid leukemia cell line K562 / ADM and to explore the relationship between this effect and the PI-3K / Akt signaling pathway. Methods Selenium chitosan treatment of K562 / ADM cells, MTT assay and colony formation assay of selenium chitosan on cell proliferation and survival effects, calculate the fold fold; Western blot was used to detect p-Akt protein expression changes . Results As the concentration of selenized chitosan increased, the inhibition rate of cell proliferation increased correspondingly, and the survival rate decreased correspondingly, showing a dose-time effect relationship. Selenized chitosan could down-regulate the expression of p-Akt (P <0.01) and enhance the inhibitory effect of ADM on the proliferation of K562 / ADM cells (P <0.05, P <0.01). Conclusion Selenium chitosan can inhibit the proliferation and multidrug resistance of K562 / ADM cells by inhibiting PI-3K / Akt signaling pathway.