细胞外信号调节激酶抑制剂协同蟾蜍灵诱导K562细胞凋亡

目的 观察细胞外信号调节激酶(extracellular signal-regulated kinases, ERK )抑制剂PD98059与蟾蜍灵(bufalin)协同诱导K562细胞凋亡作用并探讨其分子机制.方法 采用台盼蓝拒染法测定细胞增殖活力;采用形态学观察和流式细胞仪检测细胞凋亡;Western blot方法检测bcl-2蛋白表达.结果 25～100 μmol/L 的PD98059与蟾蜍灵单独或联合应用可抑制K562细胞增殖,并诱导细胞凋亡,在此过程中下调bcl-2蛋白表达,且二者具有协同作用.结论 PD98059协同蟾蜍灵诱导K562细胞凋亡,其机制可能与下调bcl-2蛋白表达有关.

ERK inhibitor synergistic with bufalin induces K562 cells' apoptosis

Objective To observe the synergistic effects of extracellular signal regulated kinase (ERK) inhibitor PD98059 and bufalin on the apoptosis of K562 cells. Methods The percentage of viable cells was determined by trypan blue exclusion. Cell apoptosis was examined by morphology and flow cytometry, and the bcl-2 protein was measured by western blot analysis. Results ERK inhibitor alone inhibited the proliferation of cells, downregulated bcl-2 protein and induced apoptosis of K562 cells; bufalin was proved to have synergistic effect on the PD98059-induced apoptosis, and downregulated bcl-2 protein markedly. Conclusion PD98059 has synergistic effect with bufalin to induce the apoptosis of K562 cells, probably by the mechanism of bcl-2 protein downregulation.