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曲格列酮,一种过氧化物酶体增殖物激活受体γ配体,可诱导人肝癌细胞HepG2的生长抑制和凋亡。

Troglitazone, a peroxisome proliferator-activated receptor gamma ligand, induces growth inhibition and apoptosis of HepG2 human liver cancer cells.

作者信息

Zhou Yan-Ming, Wen Yin-Hao, Kang Xiao-Yan, Qian Hai-Hua, Yang Jia-Mei, Yin Zheng-Feng

机构信息

Department of Molecular Oncology, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai 200438, China.

出版信息

World J Gastroenterol. 2008 Apr 14;14(14):2168-73. doi: 10.3748/wjg.14.2168.

DOI:10.3748/wjg.14.2168
PMID:18407589
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2703840/
Abstract

AIM

To examine the effect of troglitazone, a peroxisome proliferator-activated receptor gamma (PPAR gamma) ligand, on the proliferation and apoptosis of human liver cancer cells.

METHODS

Liver cancer cell line HepG2 was cultured and treated with troglitazone. Cell proliferation was detected by 3-(4-,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay; apoptosis was detected by flow cytometry and terminal deoxynucleotidyl transferase-mediated nick end labeling of DNA fragmentation sites (TUNEL) assay; and apoptosis-related protein was detected by immunocytochemistry and Western blotting.

RESULTS

Troglitazone inhibited growth and induced apoptosis of HepG2 cells in a dose-dependent manner, and induced activation of caspase-3 expression. Troglitazone not only drove apoptosis-inhibiting factor survivin to translocate incompletely from the nucleus to the cytoplasm, but also inhibited expression of survivin, while it did not affect expression of apoptosis-promoting factor Bax.

CONCLUSION

PPAR gamma ligands inhibit growth and induce apoptosis of liver cancer cells, and may have applications for the prevention and treatment of liver cancer.

摘要

目的

研究过氧化物酶体增殖物激活受体γ(PPARγ)配体曲格列酮对人肝癌细胞增殖和凋亡的影响。

方法

培养肝癌细胞系HepG2并用曲格列酮处理。通过3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐(MTT)法检测细胞增殖;通过流式细胞术和脱氧核糖核苷酸末端转移酶介导的DNA片段末端标记(TUNEL)法检测凋亡;通过免疫细胞化学和蛋白质免疫印迹法检测凋亡相关蛋白。

结果

曲格列酮以剂量依赖性方式抑制HepG2细胞生长并诱导其凋亡,且诱导半胱天冬酶-3表达激活。曲格列酮不仅促使凋亡抑制因子生存素从细胞核向细胞质不完全转位,还抑制生存素表达,而对促凋亡因子Bax表达无影响。

结论

PPARγ配体抑制肝癌细胞生长并诱导其凋亡,可能在肝癌防治中具有应用价值。

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