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[辛伐他汀对HepG2细胞增殖的影响]

[Effects of simvastatin on the proliferation of HepG2 cells].

作者信息

Liu Wei, Zhang Lian-feng, Zhang Yu-heng

机构信息

Department of Gastroenterology, the First Hospital of Zhengzhou University, Zhengzhou 450052, China.

出版信息

Zhonghua Gan Zang Bing Za Zhi. 2010 Oct;18(10):751-3. doi: 10.3760/cma.j.issn.1007-3418.2010.10.007.

DOI:10.3760/cma.j.issn.1007-3418.2010.10.007
PMID:21059291
Abstract

OBJECTIVE

To investigate the effects of simvastatin on the proliferation, cell cycle and expression of cyclin-dependent kinase inhibitor p21 protein in human hepatocellular carcinoma (HepG2) cells in vitro.

METHODS

HepG2 cells were administrated with simvastatin. Proliferation of the cells was detected by MTT assay, cell cycle was measured by flowcytometry and the cyclin-dependent kinase inhibitor p21 protein expression was detected by immunocytochemistry. The results were evaluated by factorial design and one-way analysis of variance.

RESULTS

Simvastatin inhibited HepG2 cells growth in vitro (F(concentration) = 1264, P value less than 0.001; F(time) = 17.466, P value less than 0.001; F(concentration*time) = 35.053, P value less than 0.001) and could arrest HepG2 cells in G0/G1 phase of cell cycle. However, apoptosis of HepG2 cells was not obvious. Simvastatin could also increase cyclin-dependent kinase inhibitor p21 protein expression (F = 512.133, P value less than 0.001).

CONCLUSION

Simvastatin can inhibit the growth of HepG2 cells in vitro, which may be explained by its effects of enhancing cyclin-dependent kinase inhibitor p21 protein expression and arresting HepG2 cells at G0/G1 phase of cell cycle.

摘要

目的

研究辛伐他汀对人肝癌(HepG2)细胞体外增殖、细胞周期及细胞周期蛋白依赖性激酶抑制剂p21蛋白表达的影响。

方法

用辛伐他汀处理HepG2细胞。采用MTT法检测细胞增殖,流式细胞术检测细胞周期,免疫细胞化学法检测细胞周期蛋白依赖性激酶抑制剂p21蛋白表达。结果采用析因设计和单因素方差分析进行评价。

结果

辛伐他汀在体外抑制HepG2细胞生长(F(浓度)=1264,P值<0.001;F(时间)=17.466,P值<0.001;F(浓度×时间)=35.053,P值<0.001),并可使HepG2细胞停滞于细胞周期的G0/G1期。然而,HepG2细胞的凋亡并不明显。辛伐他汀还可增加细胞周期蛋白依赖性激酶抑制剂p21蛋白表达(F=512.133,P值<0.001)。

结论

辛伐他汀可在体外抑制HepG2细胞生长,这可能与其增强细胞周期蛋白依赖性激酶抑制剂p21蛋白表达及使HepG2细胞停滞于细胞周期的G0/G1期的作用有关。

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