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目的:探讨酪氨酸激酶抑制剂伊马替尼联合槲皮素诱导K562细胞凋亡的机制。方法:将250 nmol/L的伊马替尼、25μmol/L的槲皮素单药及联合作用于K562细胞,通过细胞计数检测细胞增殖,流式细胞仪分析细胞凋亡,蛋白印迹法检测相关蛋白的表达。结果:250 nmol/L伊马替尼联合25μmol/L槲皮素对K562细胞有明显的协同诱导凋亡作用,两药联合较单药处理能明显协同下调p-BCR/ABL、p-Crkl蛋白的表达。结论:伊马替尼和槲皮素协同诱导K562细胞凋亡,其机制可能是主要通过协同抑制BCR/ABL蛋白磷酸化水平,从而抑制下游信号通路的激活,导致细胞凋亡。
AIM: To investigate the mechanism of tyrosine kinase inhibitor imatinib combined with quercetin inducing apoptosis in K562 cells. METHODS: K562 cells were treated with 250 nmol / L imatinib and 25 μmol / L quercetin alone. Cell proliferation was measured by cell counting. Apoptosis was analyzed by flow cytometry and Western blotting Protein expression. Results: The combination of 250 nmol / L imatinib and 25 μmol / L quercetin could obviously induce the apoptosis of K562 cells. The combination of the two drugs significantly reduced the expression of p-BCR / ABL and p-Crkl protein expression. CONCLUSION: Imatinib and quercetin can induce the apoptosis of K562 cells synergistically. The mechanism may be that synergistically inhibit the phosphorylation of BCR / ABL protein and inhibit the activation of downstream signaling pathway, leading to apoptosis.