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目的研究藤黄酸对人慢性粒细胞性白血病细胞株K562抑制增殖及诱导凋亡的作用,并探讨其可能作用机制。方法用藤黄酸处理K562细胞,采用MTS法和台盼兰计数法测定细胞活力及增殖;碘化丙啶(PI)单染荧光显微镜观察细胞形态改变;采用AnnexinV-FTIC/PI流式细胞术检测细胞凋亡;利用Western blotting检测凋亡相关蛋白及细胞增殖信号通路的变化情况。结果藤黄酸对K562细胞的增殖抑制作用呈时间和浓度依赖性(P<0.05)。藤黄酸处理后的细胞,经PI染色,荧光显微镜下观察可见死亡细胞形态发生改变,细胞核红染。流式细胞术检测显示加药处理组细胞以凋亡方式为主,凋亡率比对照组明显升高(P<0.05)。Western blotting检测发现凋亡相关蛋白激活,Bcr-Abl及下游的信号通路受到不同程度的抑制(P<0.05)。结论藤黄酸对K562细胞具有凋亡诱导和增殖抑制作用,作用机制与caspase系统激活和Bcr-Abl增殖相关通路受抑有关。
Objective To study the effects of gambogic acid on the proliferation and apoptosis of human chronic myelogenous leukemia cell line K562 and to explore its possible mechanism. Methods K562 cells were treated with gambogic acid, cell viability and proliferation were measured by MTS assay and trypan blue counting method. Morphological changes were observed by single staining with propidium iodide (PI) fluorescent microscope. Annexin V-FTIC / PI flow cytometry Apoptosis was detected. Western blotting was used to detect the changes of apoptosis related proteins and cell proliferation signal pathways. Results Gambogic acid inhibited the proliferation of K562 cells in a time and concentration-dependent manner (P <0.05). Gambogic acid-treated cells, PI staining, under the fluorescence microscope shows the morphological changes of dead cells, the nucleus red dye. Flow cytometry showed that the apoptotic rate was higher in the drug-treated group than in the control group (P <0.05). Apoptosis-related protein activation was detected by Western blotting, and the signal pathways of Bcr-Abl and downstream were inhibited to some extent (P <0.05). Conclusion Gambogic acid can induce the apoptosis of K562 cells and inhibit the proliferation of K562 cells. The mechanism is related to the inhibition of caspase activation and the proliferation of Bcr-Abl.