摘要
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。
Objective： To investigate the synergistic effect of imatinib combined with quercetin on K562 cell line. Methods： K562 cells were treated with imatinib （250 nmol/L）and quereetin （25 umol/L） alone or both. Cell proliferation was assayed by cell count, apoptosis was detected by flow cytometry, and expression of related protein was measured by Westernblotting. Results： Quereetin combined with imatinib could synergistically induce cell apoptosis in K562 cells, and synergistically down-regulate the expressions of p-BCR/ABL and p-Crkl protein. Conclusions： Imatinih combined with- quercetin could synergistically induce the apoptosis of K562 cells, probably by inhibiting the phosphorylation level of BCR/ABL protein, thereby inhibiting the the activation of down-stream signal pathway and inducing apoptosis.
出处
《诊断学理论与实践》
2013年第6期610-613,共4页
Journal of Diagnostics Concepts & Practice
基金
国家自然科学基金(81170508)
上海市科委优秀学术带头人计划项目(11XD1403500)
