千层纸素诱导人慢性粒细胞白血病K562的凋亡作用

Apoptosis induction of oroxylin A in human chronic myelogenous leukemia cell line K562

探讨千层纸素对人慢性粒细胞白血病细胞K562的凋亡诱导作用及其可能机制。采用MTT法检测细胞存活率;电镜下观察细胞超微结构的改变;DAPI染色观察细胞凋亡;流式细胞仪检测细胞凋亡率;Western blot法分析凋亡相关蛋白caspase 9、survivin及ERK1/2的表达变化情况。结果表明千层纸素呈浓度依赖地抑制K562细胞的增殖作用,诱导K562细胞发生凋亡,上调K562细胞中cleaved-caspase 9蛋白,下调survivin、pro-caspase 9及p-ERK1/2蛋白的表达水平。千层纸素可诱导K562凋亡,这可能与下调survivin蛋白表达,激活caspase 9蛋白,抑制ERK信号通路有关。

To investigate the apoptotic effect of oroxylin A on human chronic myelogenous leukemia cell line K562 and its potential mechanism. K562 cells were treated with oroxylin A. MTr assay was performed to assess growth inhibition effect of oroxylin A on K562 cells. The morphological change of cells were observed under electronic microscope. DAPI staining and flow cytometry were employed to observe the apoptosis rate of K562 cells. Changes in the expression of caspase 9, survivin and ERK1/2 were analyzed by Western blotting. Results showed that oroxylin A inhibited the growth of K562 in a time and dose-dependent manner. Oroxylin A induced cell apoptosis was characterized by appearance of numerous engorged vacuoles, reduction of microvilli on cell surface, condensation of chromatin and emergence of apoptotic body. Besides, oroxylin A dose-dependently induced K562 cell apoptosis, up-regulated the expression of cleaved-caspase 9 and down-regulated expression of survivin, pro-caspase 9 and p-ERK1/2 proteins. In conclusion, all these results showed that oroxylin A can induce apoptosis of K562 inhibition of cells, which might be related to the down-regulation of survivin expression, activation of caspase 9 and ERK signaling pathway