Original Articles
Copyright ©2009 The WJG Press and Baishideng. All rights reserved.
World J Gastroenterol. Apr 14, 2009; 15(14): 1751-1758
Published online Apr 14, 2009. doi: 10.3748/wjg.15.1751
Exogenous phosphatidylethanolamine induces apoptosis of human hepatoma HepG2 cells via the bcl-2/bax pathway
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
Yu Yao, Department of Oncology, First Affiliated Hospital of Medical College of Xi’an Jiaotong University, Xi’an 710061, Shaanxi Province, China
Yu Yao, Chen Huang, Ai-Ying Wang, Li-Ying Liu, Xiao-Ge Zhao, Yu Luo, Lei Ni, Tu-Sheng Song, 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
Zong-Fang Li, Wang-Gang Zhang, 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
Author contributions: Yao Y and Huang C performed the majority of experiments; Yao Y, Huang C and Song TS designed the research; Li ZF, Zhang WG and Liu LY provided the vital reagents and analytical tools and were involved in editing the manuscript; Wang AY, Zhao XG, Luo Y, Ni L analyzed the data.
Correspondence to: Chen Huang, 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. hchen@mail.xjtu.edu.cn
Telephone: +86-29-82657723
Fax: +86-29-82655077
Received: December 29, 2008
Revised: March 13, 2009
Accepted: March 20, 2009
Published online: April 14, 2009
Abstract

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 dose- and time- dependent manner. It did not affect 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 dose- and time-dependent manner.

CONCLUSION: Exogenous PE induces apoptosis of human hepatoma HepG2 cells via the bcl-2/bax pathway.

Keywords: Apoptosis; Bcl-2; Bax; Caspase-3; Phosphatidylethanolamine; Human hepatoma HepG2 cell