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作 者:王甦[1] 张晓晶[1] 刘云鹏[1] 侯科佐[1] 罗颖[1] 刘世洲[1]
机构地区:[1]中国医科大学附属第一医院肿瘤内科,沈阳110001
出 处:《第三军医大学学报》2007年第5期393-395,共3页Journal of Third Military Medical University
基 金:辽宁省自然科学基金(20022077);辽宁省教育厅基金(20122152)~~
摘 要: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25~100μmol/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。Objective To observe the synergistic effects of extracellular signal regulated kinase (ERK) inhibitor PD98059 and bufalin on the apoptosis of K562 ceils. Methods The percentage of viable ceils 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 ceils, downregulated bcl-2 protein and induced apoptosis of K562 ceils; 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 ceils, probably by the mechanism of bcl-2 protein downregulation.
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