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阿魏酸促进人骨肉瘤细胞系凋亡。

Ferulic acid promoting apoptosis in human osteosarcoma cell lines.

作者信息

Zhang Xu-Dong, Wu Qiang, Yang Shu-Hua

机构信息

Dr. Xu-dong Zhang, Department of Orthopedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Prof. Qiang Wu, Department of Orthopedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

出版信息

Pak J Med Sci. 2017 Jan-Feb;33(1):127-131. doi: 10.12669/pjms.331.12066.

DOI:10.12669/pjms.331.12066
PMID:28367185
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5368292/
Abstract

OBJECTIVE

To explore the promoting apoptosis and antitumor activities of ferulic acid (FA) in human osteosarcoma and its potential mechanism.

METHODS

The SaOS-2 and MG63 osteosarcoma cell lines were opted to experiment and these cells were, respectively, cultured with various concentrations of FA (0 μM, 10 μM, 20 μM, 40 μM) for 72 hours at 37°C. The viabilities of the FA treated cells were monitored by MTT. Apoptosis cells were evaluated using annexin V/PI by flow cytometry. Apoptosis proteins caspase-3, procaspase-3, Bcl-2 and Bax were detected by western blot. Expressions of apoptotic genes Bcl-2 and Bax were quantified by qPCR.

RESULTS

The cell viabilities were critically declined in the concentration-dependent manner in FA groups ( < 0.01). The apoptosis cells were increased proportionately with the concentration of FA ( < 0.05). The procaspase-3 protein contents, and Bcl-2 mRNA and protein contents were significantly decreased while caspase-3 protein contents, and Bax mRNA and protein contents were concomitantly increased in the concentration-dependent manner in FA groups ( < 0.05). The response to FA by the SaOS-2 osteosarcoma cell was similar with the MG63 osteosarcoma cell ( > 0.05).

CONCLUSION

Ferulic acid could significantly descend osteosarcoma cell viability through the promoting apoptosis pathway in which FA activates both caspase-3 and Bax and inactivates Bcl-2.

摘要

目的

探讨阿魏酸(FA)对人骨肉瘤细胞的促凋亡及抗肿瘤活性及其潜在机制。

方法

选用SaOS-2和MG63骨肉瘤细胞系进行实验,将这些细胞分别用不同浓度的FA(0 μM、10 μM、20 μM、40 μM)在37℃培养72小时。采用MTT法监测FA处理后细胞的活力。通过流式细胞术使用膜联蛋白V/PI评估凋亡细胞。通过蛋白质免疫印迹法检测凋亡蛋白caspase-3、procaspase-3、Bcl-2和Bax。通过qPCR定量凋亡基因Bcl-2和Bax的表达。

结果

FA组细胞活力呈浓度依赖性显著下降(<0.01)。凋亡细胞随FA浓度成比例增加(<0.05)。FA组procaspase-3蛋白含量、Bcl-2 mRNA和蛋白含量显著降低,而caspase-3蛋白含量、Bax mRNA和蛋白含量呈浓度依赖性增加(<0.05)。SaOS-2骨肉瘤细胞对FA的反应与MG63骨肉瘤细胞相似(>0.05)。

结论

阿魏酸可通过促进凋亡途径显著降低骨肉瘤细胞活力,其中FA激活caspase-3和Bax并使Bcl-2失活。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8ea/5368292/b4d645cb4249/PJMS-33-127-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8ea/5368292/2503d7629ced/PJMS-33-127-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8ea/5368292/fae4337440c5/PJMS-33-127-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8ea/5368292/b4d645cb4249/PJMS-33-127-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8ea/5368292/2503d7629ced/PJMS-33-127-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8ea/5368292/fae4337440c5/PJMS-33-127-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8ea/5368292/b4d645cb4249/PJMS-33-127-g003.jpg

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