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.
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DOI：
10.3748/wjg.15.1751
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发表时间：
2009-04
影响因子：
4.3
通讯作者：
Yu Yao;Chen Huang;Zong-fang Li;Ai-ying Wang;Liying Liu;Xiao-ge Zhao;Yu Luo;L. Ni;Wanggang Zhang;T. Song
中科院分区：
文献类型：
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作者：
Yu Yao;Chen Huang;Zong-fang Li;Ai-ying Wang;Liying Liu;Xiao-ge Zhao;Yu Luo;L. Ni;Wanggang Zhang;T. Song
目的探讨磷脂酰乙醇胺(PE)诱导人肝癌细胞HepG2凋亡的信号转导途径。方法采用四甲基偶氮唑蓝(3-(4，5-dimethylthiazol-2-yl)-2，5-diphenyltetrazolium)比色法检测PE对人肝癌细胞的抑制作用。流式细胞仪检测细胞周期、细胞凋亡率和线粒体跨膜电位(DeltaPsi M)。采用免疫细胞化学法和Western blotting法检测PE作用后HepG2细胞中Bcl2、Bax和caspase 3蛋白的表达。结果PE对HepG2细胞生长有抑制作用，且呈剂量和时间依赖性。对细胞周期无影响，但可诱导细胞凋亡。PE0.25、0.5和1 mmol/L可显著降低DeltaPsim，提示PE通过降低线粒体跨膜电位而诱导细胞凋亡。不同浓度PE诱导的Bcl2表达水平均低于对照组。而PE诱导的Bax表达水平明显高于对照组。同时，PE以剂量和时间依赖的方式增加caspase-3的表达。结论外源性PE通过bcl2/bax途径诱导人肝癌细胞株HepG2细胞凋亡。
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 (DeltaPsi m) 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 DeltaPsi m 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.