中文摘要：

目的观察α-硫辛酸（α-LA）拮抗氯化镉（CdCl2）致HepG2细胞氧化损伤的保护作用。方法本实验以HepG2细胞为研究对象,CdCl2诱导细胞产生氧化损伤模型。实验分组如下：正常对照组、CdCl2单独作用组、α-LA单独作用组和α-LA＋CdCl2联合作用组,用含不同浓度梯度α-LA（1μM、5μM、50μM）的培养液体外培养HepG2细胞8 h,再加入终浓度为25μM CdCl2,采用MTT法检测细胞存活率,彗星实验检测DNA损伤,并同时检测细胞内活性氧（ROS）水平和脂质过氧化产物丙二醛（MDA）含量。结果与正常对照组相比,细胞经CdCl2诱导处理后,细胞存活率（0.814±0.756）降低,胞内ROS水平（987.18±14.529）增高,MDA含量（1.256 3±0.964）增加,DNA（4.398±1.068）损伤严重。不同浓度（1μM、5μM、50μM）α-LA预处理后能减轻CdCl2所致的细胞损伤[（0.843±0.658）,（0.906±0.469）,（0.954±1.163）],减少胞内ROS[（973.40±26.581）,（935.49±14.358）,（920.60±6.023）]累积,减轻脂质过氧化反应[（0.973 4±0.154）,（0.672 9±0.125）,（0.534 3±0.156）]及DNA损伤[（4.263±0.093）,（3.764±0.087）,（2.659±0.116）]的程度,且与α-LA浓度之间呈剂量-效应关系。结论α-LA可以拮抗CdCl2致HepG2细胞氧化应激,降低CdCl2诱导HepG2细胞产生的氧化损伤。

英文摘要：

Objective To determine the antagonistic effect of α-lipoic acid（α-LA） on the oxidative damage of HepG2 cells exposed to Cadmium Chloride.Methods we use HepG2 cells in the experiment,then induced by Cadmium Chloride to produce oxidative damage model.The whole cells were divided into normal group,Cadmium Chloride group and α-LA pre-treatment groups.Cells were cultured in vitro and treated with different concentrations ofα-LA（1μM,5μM,50 μM） incubated for 8 hours,then treated with CdCl2（25 μM） MTT assay was uesd to measure the cell viability,Comet assay was employed to evaluate the levels of DNA,The assay kits of intracellular reactive oxygen species（ROS） and malondialdehyde（MDA） were used to detect the alterations of oxidative stress.Results Compared with the normal control,the cell viability（0.814±0.756） was decreased,the intracellular ROS levels（987.18±14.529）,MDA contents（1.256 3±0.964）and the damage of DNA（4.398±1.068） were increased in CdCl2-induce group;After pre-treatment with different concentration of α-LA,the cell viability[（0.843±0.658）,（0.906±0.469）,（0.954±1.163）]were relieved,the intracellular ROS levels[（973.40±26.581）,（935.49±14.358）,（920.60±6.023）]accumulation,lipid peroxidative[（0.9734±0.154）,（0.6729±0.125）,（0.5343±0.156）]and the damage of DNA[（4.263±0.093）,（3.764±0.087）,（2.659±0.116）]were decreased in co-treatment groups.And at the same time this tendency has a dose-relationship with the concentration of α-LA.Conclusion ct-LA can antagonize oxidative stress and alleviate the cytotoxicity induced by Cadmium Chloride in HepG2 cells.