摘要
目的研究不同浓度4-邻氨基酚-4'去甲表鬼臼酯(ODE)对肿瘤细胞生长的影响,探讨ODE诱导肿瘤细胞凋亡的机制。方法采用MTT法测定ODE对K562细胞生长的抑制作用,透射电镜观察细胞超微结构,免疫细胞化学方法检测K562细胞中Bcl-2/Bax比率变化。结果 (1)不同浓度ODE对K562细胞生长有抑制作用,随ODE浓度的增加及作用时间的延长细胞生长抑制率增高(P<0.05);(2)透射电镜观察可见凋亡细胞发生;(3)凋亡细胞中Bcl-2灰度较正常细胞染色的灰度低,Bax在凋亡细胞中的灰度较正常细胞高。结论 ODE能够显著抑制K562细胞的生长,其抑制作用随浓度的增加及时间的延长而增强,通过形态学可观察到凋亡细胞的产生,其诱导凋亡可能是通过改变凋亡基因而发挥作用的。
Objective To study the apoptosis of K562 cell line induced by 4 - o - aminophenol - 4＇ - demethylepipoph- yliotoxin ester（ODE） thus exploring mechanisms of ODE induce tumor cells apoptosis. Methods The cell growth and proliferation were measured by MTT assay method. Cell apoptosis were evaluated by transmission electronmicroscope（TEM） ,the expression of cell apoptosis associated genes were examined by inmunohistochemical staining. Results （ 1 ） ODE of different concen- trations control growth of K562 cells considerably,with an increase in the concentration of ODE and the extension of the time,cell growth disincentive rate increases（ P 〈 0.05 ）. （2）TEM observate apoptosis cells. （3）Apoptosis cells Bcl -2 using （colour diff- cuhion） than normal cells staining of using low,Bax in apoptosis cells than that in normal cells,using high. Conclusion ODE can significantly inhibit the growth of K562 cells,with an increase in the concentration of ODE and the extension of the time, cell growth disincentive rate increases. ODE may lead to cells apoptosis through regulation of genes and ceils.
出处
《中国医学创新》
CAS
2010年第26期5-7,共3页
Medical Innovation of China
