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Exogenous phosphatidylethanolamine induces apoptosis of human hepatoma HepG2 cells via the bcl-2/bax pathway

Exogenous phosphatidylethanolamine induces apoptosis of human hepatoma HepG2 cells via the bcl-2/bax pathway

作     者:Yu Yao Chen Huang Zong-Fang Li Ai-Ying Wang Li-Ying Liu Xiao-Ge Zhao Yu Luo Lei Ni Wang-Gang Zhang Tu-Sheng Song 

作者机构:Department of Oncology First Affiliated Hospital of Medical College of Xi'an Jiaotong University Xi'an 710061 Shaanxi Province China Department of Genetics and Molecular Biology Medical School Xi'an Jiaotong University/Key Laboratory of Environment and Genes Related to Diseases Ministry of Education Xi'an 710061 Shaanxi Province China Second Affiliated Hospital of Xi'an Jiaotong University/Key Laboratory of Environment and Genes Related to Diseases Ministry of Education Xi'an 710004 Shaanxi Province China 

出 版 物:《World Journal of Gastroenterology》 (世界胃肠病学杂志(英文版))

年 卷 期:2009年第15卷第14期

页      面:1751-1758页

核心收录:

学科分类:1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

基  金:Supported by The National Natural Science Foundation of China (No. 30872481) the Scientific and Technological Planning Foundation of Shaanxi Province (No. 2006K09-G7-1) 

主  题:Apoptosis Bcl-2 Bax Caspase-3 Phosphatidylethanolamine Human hepatoma HepG2 cell 

摘      要:AIM: To investigate the signaling pathways implicated in phosphatidylethanolamine (PE)-induced apoptosis of human hepatoma HepG2 cells. METHODS: Inhibitory effects of PE on human hepatoma HepG2 cells were detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Cell cycle, apoptosis and mitochondrial transmembrane potential (ΔΨm) were analyzed by flow cytometry. Immunocytochemical assay and Western blotting were used to examine Bcl-2, Bax and caspase-3 protein levels in HepG2 cells treated with PE. RESULTS: PE inhibited the growth of HepG2 cells in a doseand timedependent manner. It did notaffect the cell cycle, but induced apoptosis. PE significantly decreased ΔΨm at 0.25, 0.5 and 1 mmol/L, respectively, suggesting that PE induces cell apoptosis by decreasing the mitochondrial transmembrane potential. The Bcl-2 expression level induced by different concentrations of PE was lower than that in control groups. However, the Bax expression level induced by PE was higher than that in the control group. Meanwhile, PE increased the caspase-3 expression in a doseand time-dependent manner. CONCLUSION: Exogenous PE induces apoptosis of human hepatoma HepG2 cells via the bcl-2/bax pathway.

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