目的研究芒果苷诱导慢粒白血病细胞系K562细胞凋亡的机制。方法采用RT-PCR检测芒果苷(25~200μmol/L)处理(24、48、72、96h)后K562细胞中bcl-2 mRNA、bax mRNA、survivin mRNA基因表达变化;采用Western blotting方法检测K562细胞BCR/ABL融合蛋白质P210水平。结果芒果苷作用K562细胞后,P210蛋白质水平下调,并呈时间及剂量依赖性,bax基因表达显著上调,bcl-2基因表达轻度下调,survivin mRNA基因表达下调。结论芒果苷诱导K562细胞凋亡的机制可能是通过下调BCR/ABL融合蛋白质P210、bcl-2和sur-vivin mRNA基因表达及上调bax基因表达来实现的。

Objective To study the apoptosis mechanism of K562 cell lines induced by mangiferin.Methods The mRNA expression levels of apoptosis-related genes including bcl-2,bax,survivin of K562 cells treated by mangiferin (25-200 μmol/L) for 24,48,72,and 96 h were determined by RT-PCR; the BCR/ABL protein P210 level was detected by Western blotting.Results Mangiferin up-regulated bax gene of K562 cells significantly and down-regulated bcl-2 gene slightly,resulting in an enhancement of the ratio of bax/bcl-2.Mangiferin down-regulated the expression levels of P210 in K562 cells in a time-and concentration-dependent manner and so is the expression level of survivin mRNA in K562 cells.ConclusionThe mechanism of mangiferin-induced apoptosis in K562 leukemic cells might be involved in up-regulating the gene expression of bax and down-regulating the mRNA expression of BCR/ABL protein P210,bcl-2,and survivin.