人参皂苷Compound K对慢性粒细胞白血病K562细胞系凋亡诱导作用及其机制的研究

[目的]探讨人参皂苷CompoundK（CK）对慢性粒细胞白血病K562细胞凋亡的诱导作用及其机制。[方法]应用MTT法检测CK对K562细胞增殖的影响，用流式细胞术分析细胞凋亡情况，半定量RT—PCR检测Caspase3、Caspase9、Bcl-2和Bax的mRNA表达水平，WesternBlot检测Caspase3、Caspase9、Bcl-2和Bax蛋白质的表达。[结果]人参皂苷CK能诱导K562细胞的凋亡，细胞凋亡率呈浓度依赖性增加。RT—PCR结果显示Caspase3、Caspase9mRNA的表达上调，Bcl-2mRNA的表达下调，WesternBlot实验显示蛋白质表达情况与RT—PCR结果-致，Caspase3、Caspase9蛋白质的表达上调，Bcl-2的表达下调。[结论]人参皂苷CK诱导K562细胞凋亡作用的机制可能是CK抑制Bcl-2基因的表达，进而使Caspase3、Caspase9表达量上调，启动凋亡途径，引起凋亡。

Effect of Apoptosis Inducing of Ginsenoside Compound K on Chronic Myelocytic Leukemia K562 Cells and Its Mechanism

[Purpose] To investigate the apoptosis of Ginsenoside CK on the K562 cells and its mechanism. [Methodsl The proliferation inhibition effects of Ginsenoside CK on the K562 cells were determined by MTT assay. K562 cells apoptotic percentage was detected by flow cytometry. The mRNA expression of Caspase3, Caspase9, Bcl-2 and Bax was detected by semi-quantitative RT-PCR. Western Blot assay was carried out to examine Caspase3, Caspase9,Bcl-2 and Bax protein expression. [Results ] Ginsenoside CK significantly in- hibited the proliferation of K562 cells in dose-dependent and time-dependent manners. In addition ,apoptosis percentage of K562 cells can be induced by Ginsenoside CK in dose-dependent manner. The expression of Caspase3, Caspase9 mRNA was obviously up-regulated,while the Be1-2 expression was down-regulated. The result of Western Blot assay was accord with that of RT-PCR. The expression of Caspase3, Caspase9 protein was obviously up-regulated,while the Bcl-2 expression was down-regulated. [Conclusion] Ginsenoside CK plays a crucially important role in exerting its anti-leukemic effects via induction of apoptosis in K562 cells. This effect is possibly to inhibit Bcl-2 expression,which may occur apoptosis through decreasing Bcl-2 expression down-regulated by caspase pathway.