当归多糖诱导K562白血病细胞凋亡的实验研究

目的从细胞凋亡的角度探讨当归多糖(APS)抑制白血病细胞增殖的机制。方法体外培养白血病细胞株K562,培养时添加25 mg/L、250 mg/L、2 500 mg/L当归多糖,分别于第2,4,6天,取细胞用台盘蓝拒染法进行活细胞计数;流式细胞术分析细胞周期分布;免疫组织化学检测bcl-2抗凋亡基因的表达。结果细胞生长曲线显示25~2 500 mg/L的当归多糖对白血病细胞株K562有显著抑制作用,且呈剂量效应关系。流式细胞术结果显示250 mg/L作用后S,G2+M期K562细胞数减少,G0/G1期细胞增多。APS诱导细胞后bcl-2明显降低(P<0.05)。结论APS对白血病细胞株K562细胞的增殖具有显著抑制作用,APS通过阻止K562细胞进入S期而抑制其DNA合成,bcl-2表达降低可能是APS诱导白血病细胞凋亡重要途径之一。

Empirical study of angelica polysaccharide inducting apoptosis of K562 leukemic cell

Objective It is to discuss the mechanism of angelica polysaccharide(APS) inhibiting proliferation of leukemic cell from the angulation of apoptosis.Methods K562 leukemic cell were cultured in vitro and 25 mg/L,250 mg/L and 2?500 mg/L APS were added.Cell counting,cell cycle distribution and bcl-2 anti-apoptosis gene expression were analyzed with flow cytometry and Immunohistochemistry method at the second,fourth and sixth day.Results Cell growth curve showed 25～2?500 mg/L APS had significant inhibition action on K562 leukemic cell and the relation was dose dependent.Flow cytometry result showed after 250 mg/L APS given,the S phase and G_2+M phase K562 cells decreased and the G_0/G_1 phase K562 cells increased.After APS induced,bcl-2 expression obviously lowered(P<0.05).Conclusion APS can significantly inhibit proliferation of K562 leukemic cells.APS inhibits its DNA synthesis through preventing K562 cell to enter S phase.Bcl-2 expression lower may be an important path of APS inhibiting leukemic cell apoptosis.