叶黄素对人肝癌细胞HepG2的抑制作用及其机制研究

STUDY ON THE INHIBITION OF LUTEIN ON HUMAN HEPATOMA CELL HepG2 AND ITS MECHANISM

目的研究叶黄素对人肝癌细胞的抑制作用并探讨其可能机制。方法以HepG2人肝癌细胞株和L02正常人肝细胞株为研究对象,设叶黄素低、中、高剂量组(20、40、80 mol/L)和溶剂对照组。常规细胞培养后进行细胞计数、MTT法测定细胞存活率、DCFH-DA法测定ROS活性、HPLC法测定ATP含量、RT-PCR测定Bax mRNA及p53mRNA表达水平。结果 HepG2细胞经叶黄素干预处理后,低、中、高剂量组的细胞存活率显著降低(P<0.05),并且随干预时间的增加而持续降低,ROS水平和ATP含量显著降低(P<0.05);高剂量组的Bax mRNA表达和中、高剂量组的p53 mRNA表达显著增加(P<0.05)。而L02细胞经叶黄素干预处理后,细胞存活率和ATP含量均无显著性变化。结论叶黄素能抑制人肝癌细胞的生长,其机制可能与叶黄素清除细胞内ROS、抑制肝癌细胞ATP生成及上调凋亡基因Bax和p53 mRNA的表达有关。[营养学报,2012,34(4):332-335]

Objective To study the inhibition of lutein on human hepatoma cells and its possible mechanism.Method HepG2 and L02 cells were randomized into 4 groups： low（L-L）,middle（L-M）,high（L-H） lutein group（20,40,80 μmol/L） and control group.The cell count,survival rate,content of reactive oxygen species（ROS） and adenosine triphosphate（ATP）,mRNA expression of Bax and p53 were detected.Results With lutein treatment,HepG2 survival rates in L-L,L-M and L-H group decreased in time-dependent manner（P0.05）,ROS and ATP content decreased significantly（P0.05）,the expression of Bax mRNA in HL group and expression of p53 mRNA in ML,HL group increased significantly（P0.05）.On the other hand,with lutein treatment on L02,the survival rate and ATP content had no significant difference.Conclusion Lutein can inhibit the growth of human hepatoma cell HepG2,and the possible mechanism may be related with the effect of scavenging ROS,inhibiting ATP generation and increasing the mRNA expression of Bax and p53.