摘要
应用MTT、流式细胞仪、免疫印迹法检测全反式维甲酸(ATRA)单独或联合糖基化磷脂酰肌醇特异性磷酯酶D(GPI-PLD)特异性抑制剂1,10-二氮杂菲对肝癌细胞HepG2生物学特性的改变.ATRA使肝癌细胞HepG2 GPI-PLD基因表达及酶活性上调,并呈现剂量和时间依赖性.ATRA可抑制肝癌细胞HepG2增殖,使肝癌细胞Caspase-3表达水平显著增加,Bcl-2表达水平下调,促进肝癌细胞凋亡(P<0.05).ATRA联合1,10-二氮杂菲诱导组细胞,Bcl-2、细胞增殖活性较ATRA单独诱导组显著增强,Caspase-3、凋亡率显著下降.维甲酸可促进肝癌细胞HepG2 GPI-PLD基因表达上调,高活性的GPI-PLD有助于维甲酸抑制肝癌细胞增殖,促进肝癌细胞凋亡.
The biological characteristics change of HepG2 cells, induced by all-trans retinoic acid （ATRA） alone or combination with glycosylphosphatidylinositol specific phospholipase D （GPI-PLD） specific inhibitor 1, 10-phenanthroline, were detected by MTr, flow cytometry and Western blot. The hepatoma ceils HepG2 GPI-PLD gene expression was upregulated by ATRA in a dose and time dependent. ATRA inhibited the proliferation of HepG2 cells, decreased the Bcl-2 expression levels, increased the Caspase 3 expression lev- els and promoted hepatocellular apoptosis significantly（P〈0.05）. Compared to ATRA alone, the Bcl-2 expres- sion levels, cell proliferation activity of the HepG2 cells induced by ATRA combined 1, 10-phenanthroline were significantly increased, and the caspase-3 expression levels, apoptosis was significantly decreased. A- TRA can promote GPI-PLD gene expression in hepatoma cell HepG2 and high activity of GPI-PLD help to prevent cell proliferation and promote apoptosis of hepatoma ceils induced by ATRA.
出处
《生命科学研究》
CAS
CSCD
北大核心
2012年第1期42-47,共6页
Life Science Research
基金
国家自然科学基金资助项目(81141068)
湖南省卫生厅项目(B2006-202)
关键词
全反式维甲酸
糖基化磷脂酰肌醇特异性磷酯酶D
HEPG2细胞
all-trans retinoic acid （ATRA）
glycosylphosphatidylinositol specific phospholipase D （GPI-PLD）
HepG2 cells （Life Science Research, 2012, 16（1）： 042-047）
