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冬凌草甲素诱导PC-3细胞凋亡及其机制。

Oridonin induced the apoptosis of PC-3 cells and its mechanism.

作者信息

Li Jin, Yang Luoyan, Wu Hongtao

机构信息

Department of Urology, Central Hospital of Xiangtan, Xiangtan Hunan 411100,China.

出版信息

Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2011 Aug;36(8):754-9. doi: 10.3969/j.issn.1672-7347.2011.08.010.

Abstract

OBJECTIVE

To observe the proliferation inhibition and apoptosis promotion effect of oridonin on PC-3 cells.

METHODS

PC-3 cells were treated with different concentrations of oridonin. MTT assay and drug concentration-time survival curve were used to test the effect of oridonin on the PC-3 cells. The percentage of earlier apoptosis cells was analyzed by flow cytometry. The protein expression of caspase-3, Bcl-2, and Bax in the PC-3 cells was detected by Western blot.

RESULTS

Oridonin effectively inhibited the proliferation of PC-3 cells in both concentration- and time-dependent manner, and the IC50 of PC-3 cells was 10.29 μmol/L. HochesT(3)3258 staining and flow cytometry deteced that oridonin induced the apoptosis of PC-3 cells in a concentration-dependent manner (P<0.05). Oridonin down-regulated Bcl-2, up-regulated Bax protein, and activated caspase-3 in a concentration-dependent manner in the PC-3 cells.

CONCLUSION

The apoptosis of PC-3 cells induced by oridonin might be associated with the mitochondrial pathway.

摘要

目的

观察冬凌草甲素对PC-3细胞的增殖抑制及促凋亡作用。

方法

用不同浓度的冬凌草甲素处理PC-3细胞。采用MTT法和药物浓度-时间存活曲线检测冬凌草甲素对PC-3细胞的作用。通过流式细胞术分析早期凋亡细胞的百分比。用蛋白质免疫印迹法检测PC-3细胞中半胱天冬酶-3、Bcl-2和Bax的蛋白表达。

结果

冬凌草甲素能有效抑制PC-3细胞的增殖,呈浓度和时间依赖性,PC-3细胞的半数抑制浓度(IC50)为10.29 μmol/L。HochesT(3)3258染色和流式细胞术检测显示,冬凌草甲素呈浓度依赖性诱导PC-3细胞凋亡(P<0.05)。冬凌草甲素在PC-3细胞中呈浓度依赖性下调Bcl-2、上调Bax蛋白并激活半胱天冬酶-3。

结论

冬凌草甲素诱导PC-3细胞凋亡可能与线粒体途径有关。

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