Osthole induced proliferation inhibition and apoptosis of K562 cells by suppressing PI3K/AKT signal pathway
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摘要: 目的: 研究蛇床子素对人慢性髓系白血病细胞K562增殖和凋亡的影响,并探讨其相关作用机制。方法: 培养髓系白血病细胞K562,分别用不同浓度的蛇床子素处理(0、5、10、20 μg/ml)。细胞培养48 h后,利用MTT法检测K562细胞增殖;流式检测K562细胞凋亡;Western blot法检测PI3K、p-AKT、AKT、Bax、Bcl-2和Cleavage-Caspase3表达。结果: 蛇床子素可以呈浓度依赖性的诱导K562细胞增殖抑制和凋亡,上调Bax和Cleavage-Caspase3表达,下调PI3K、p-AKT和Bcl-2,对AKT表达无明显影响。结论: 蛇床子素可通过抑制PI3K/AKT信号通路而诱导K562细胞增殖抑制和凋亡。Abstract: Objective: To study the influence and potential mechanism of osthole in the proliferartion and apoptosis of human leukemia K562 cells.Method: The K562 cell was cultured in the DMEM.MTT method was used to evaluate the proliferation effect of K562 and the apoptosis of K562 cells were evaluated by flow cytometric analysis.The expression of PI3K,p-AKT,AKT,Bax,Bcl-2 and Cleavage-Caspase3 were detected by Western blot.Result: The osthole treatment can significantly attenuate the proliferartion rate of K562 cell,the expression of PI3K,p-AKT and Bcl-2 and increase the apoptosis rate of K562 cell,the expression of Bax and Cleavage-Caspase3.Wherefore,it had no influence on the expression of AKT.Conclusion: Osthole can induce the apoptosis and inhibit the proliferation of human leukemia K562 cells through suppressing PI3K/AKT signaling pathway.
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Key words:
- osthole /
- K562cell /
- proliferation /
- apoptosis /
- PI3K/AKT
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