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[氯化两面针碱诱导人骨肉瘤细胞凋亡及其机制]

[Nitidine chloride-induced apoptosis of human osteosarcoma cells and its mechanism].

作者信息

Xu Qiang, Li Zhao-Xu, Ye Zhao-Ming

机构信息

Department of Orthopedics, School of Medicine, Zhejiang University, Hangzhou 310009, China.

出版信息

Nan Fang Yi Ke Da Xue Xue Bao. 2011 Feb;31(2):361-4.

PMID:21354931
Abstract

OBJECTIVE

To investigate the apoptosis-inducing effect of nitidine chloride in human osteosarcoma MG-63 cells and explore its mechanism.

METHODS

The effect of nitidine chloride on the proliferation of MG-63 cells was detected by colorimetric MTT assay, and the morphological changes of cells treated with nitidine chloride were observed using fluorescence and electron microscope. Flow cytometry was performed to analyze the apoptotic rate of the cells, and the protein expression levels of caspase-3, caspase-9, Bcl-2 and Bax were detected by Western blotting.

RESULTS

Nitidine chloride inhibited the proliferation of MG-63 cells in a dose- and time-dependent manner. Fluorescence and electron microscopy revealed distinct apoptotic changes of the cells after nitidine chloride exposure. Flow cytometry indicated that nitidine chloride induced the apoptosis of MG-63 cells in a dose-dependent manner. Exposure to nitidine chloride, as shown by Western blotting, resulted in increased expressions of cleaved caspase-3, cleaved caspase-9 and Bax and decreased expressions of pro-caspase-3, pro-caspase-9 and Bcl-2.

CONCLUSION

Nitidine chloride can inhibit the proliferation of osteosarcoma cell line MG-63 by inducing cell apoptosis, the mechanism of which might be related with the activation of the caspase-dependent pathway.

摘要

目的

研究氯化两面针碱对人骨肉瘤MG-63细胞的凋亡诱导作用并探讨其机制。

方法

采用比色法MTT检测氯化两面针碱对MG-63细胞增殖的影响,利用荧光显微镜和电子显微镜观察氯化两面针碱处理后细胞的形态变化。通过流式细胞术分析细胞凋亡率,采用蛋白质印迹法检测caspase-3、caspase-9、Bcl-2和Bax的蛋白表达水平。

结果

氯化两面针碱以剂量和时间依赖性方式抑制MG-63细胞的增殖。荧光显微镜和电子显微镜显示氯化两面针碱处理后细胞出现明显的凋亡变化。流式细胞术表明氯化两面针碱以剂量依赖性方式诱导MG-63细胞凋亡。蛋白质印迹法显示,氯化两面针碱处理后,裂解的caspase-3、裂解的caspase-9和Bax表达增加,而前体caspase-3、前体caspase-9和Bcl-2表达降低。

结论

氯化两面针碱可通过诱导细胞凋亡抑制骨肉瘤细胞系MG-63的增殖,其机制可能与激活caspase依赖途径有关。

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