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 

机构地区：[1]Department of Oncology, First Affiliated Hospital of Medical College of Xi'an Jiaotong University, Xi'an 710061, Shaanxi Province, China [2]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 [3]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　　处：《World Journal of Gastroenterology》2009年第14期1751-1758,共8页世界胃肠病学杂志（英文版）

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)

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.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 （△ψm） 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 dose- and time- dependent manner. It did not affect the cell cycle, but induced apoptosis. PE significantly decreased △ψm 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 dose- and time-dependent manner. CONCLUSION： Exogenous PE induces apoptosis of human hepatoma HepG2 cells via the bcl-2/bax pathway.

关 键 词：APOPTOSIS Bcl-2 Bax Caspase-3 PHOSPHATIDYLETHANOLAMINE Human hepatoma HepG2 cell 

分 类 号：R735.7[医药卫生—肿瘤] R737.14[医药卫生—临床医学]