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Catalase protects HepG2 cells from apoptosis induced by DNA-damaging agents by accelerating the degradation of p53.过氧化氢酶通过加速p53的降解来保护HepG2细胞免受DNA损伤剂诱导的凋亡。
J Biol Chem. 2003 Feb 14;278(7):4660-7. doi: 10.1074/jbc.M206273200. Epub 2002 Dec 4.
2
Apoptosis induced in hepatoblastoma HepG2 cells by the proteasome inhibitor MG132 is associated with hydrogen peroxide production, expression of Bcl-XS and activation of caspase-3.蛋白酶体抑制剂MG132诱导肝母细胞瘤HepG2细胞凋亡与过氧化氢生成、Bcl-XS表达及半胱天冬酶-3激活有关。
Int J Oncol. 2002 Oct;21(4):857-65. doi: 10.3892/ijo.21.4.857.
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Systemic treatment of hepatocellular carcinoma.
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Pathology and pathogenesis of hepatocellular carcinoma.肝细胞癌的病理学与发病机制
Dig Dis. 2001;19(4):269-78. doi: 10.1159/000050693.
5
In vitro protective effects of Terminalia arjuna bark extracts against the 4-nitroquinoline-N-oxide genotoxicity.诃子树皮提取物对4-硝基喹啉-N-氧化物遗传毒性的体外保护作用。
J Environ Pathol Toxicol Oncol. 2002;21(1):33-44.
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Study of apoptosis in human liver cancers.人类肝癌细胞凋亡的研究。
World J Gastroenterol. 2002 Apr;8(2):247-52. doi: 10.3748/wjg.v8.i2.247.
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Structure, Recognition, and Processing of Cisplatin-DNA Adducts.顺铂-DNA加合物的结构、识别与处理
Chem Rev. 1999 Sep 8;99(9):2467-98. doi: 10.1021/cr980421n.
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Regulation and function of the p53 tumor suppressor protein.p53肿瘤抑制蛋白的调控与功能
Curr Opin Cell Biol. 2001 Jun;13(3):332-7. doi: 10.1016/s0955-0674(00)00216-7.
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Oncogenic mutations of the p53 tumor suppressor: the demons of the guardian of the genome.p53肿瘤抑制因子的致癌突变:基因组守护者的恶魔
Cancer Res. 2000 Dec 15;60(24):6788-93.
10
Growth suppression of human transformed cells by treatment with bark extracts from a medicinal plant, Terminalia arjuna.用药用植物诃子的树皮提取物处理对人转化细胞的生长抑制作用。
In Vitro Cell Dev Biol Anim. 2000 Sep;36(8):544-7. doi: 10.1290/1071-2690(2000)036<0544:GSOHTC>2.0.CO;2.

诃子树皮提取物对人肝癌细胞系HepG2凋亡的影响。

Effects of Terminalia arjuna bark extract on apoptosis of human hepatoma cell line HepG2.

作者信息

Sivalokanathan Sarveswaran, Vijayababu Marati Radhakrishnan, Balasubramanian Maruthaiveeran Periyasamy

机构信息

Department of Pharmacology and Environmental Toxicology, Dr. ALM Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai-600 113, Tamil Nadu, India.

出版信息

World J Gastroenterol. 2006 Feb 21;12(7):1018-24. doi: 10.3748/wjg.v12.i7.1018.

DOI:10.3748/wjg.v12.i7.1018
PMID:16534840
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4087891/
Abstract

AIM

To investigate the effects of Terminalia arjuna (T. arjuna) extract on human hepatoma cell line (HepG2) and its possible role in induction of apoptosis.

METHODS

Human hepatoma cells were treated with different concentrations of ethanolic extract of T. arjuna and its cytotoxicity effect was measured by trypan blue exclusion method and lactate dehydrogenase leakage assay. Apoptosis was analyzed by light and fluorescence microscopic methods, and DNA fragmentation. The mechanism of apoptosis was studied with expression of p53 and caspase-3 proteins. Glutathione (GSH) content was also measured in HepG2 cells after T. arjuna treatment.

RESULTS

T. arjuna inhibited the proliferation of HepG2 cells in a concentration-dependent manner. Apoptotic morphology was observed in HepG2 cells treated with T. arjuna at the concentrations of 60 and 100 mg/L. DNA fragmentation, accumulation of p53 and cleavage of procaspase-3 protein were observed in HepG2 cells after the treatment with T. arjuna. The depletion of GSH was observed in HepG2 cells treated with T. arjuna.

CONCLUSION

T. arjuna induced cytotoxicity in HepG2 cells in vitro. Apoptosis of HepG2 cells may be due to the DNA damage and expression of apoptotic proteins. Depletion of GSH may be involved in the induction of apoptosis of HepG2 cells.

摘要

目的

研究阿朱那诃子(Terminalia arjuna)提取物对人肝癌细胞系(HepG2)的影响及其在诱导细胞凋亡中可能发挥的作用。

方法

用不同浓度的阿朱那诃子乙醇提取物处理人肝癌细胞,通过台盼蓝排斥法和乳酸脱氢酶泄漏试验测定其细胞毒性作用。采用光学显微镜和荧光显微镜方法以及DNA片段化分析细胞凋亡情况。通过检测p53和半胱天冬酶 - 3蛋白的表达来研究细胞凋亡的机制。在阿朱那诃子处理后的HepG2细胞中还测定了谷胱甘肽(GSH)含量。

结果

阿朱那诃子以浓度依赖性方式抑制HepG2细胞的增殖。在浓度为60和100 mg/L的阿朱那诃子处理的HepG2细胞中观察到凋亡形态。用阿朱那诃子处理后的HepG2细胞中观察到DNA片段化、p53积累和前半胱天冬酶 - 3蛋白的裂解。在阿朱那诃子处理的HepG2细胞中观察到GSH的消耗。

结论

阿朱那诃子在体外对HepG2细胞具有细胞毒性作用。HepG2细胞的凋亡可能是由于DNA损伤和凋亡蛋白的表达。GSH的消耗可能参与了HepG2细胞凋亡的诱导。