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目的观察α-硫辛酸(α-LA)拮抗氯化镉(CdCl_2)致HepG_2细胞氧化损伤的保护作用。方法本实验以HepG_2细胞为研究对象,CdCl_2诱导细胞产生氧化损伤模型。实验分组如下:正常对照组、CdCl_2单独作用组、α-LA单独作用组和α-LA+CdCl_2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HepG_2细胞8 h,再加入终浓度为25μM CdCl_2,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CdCl_2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CdCl_2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CdCl_2致HepG_2细胞氧化应激,降低CdCl_2诱导HepG_2细胞产生的氧化损伤。
Objective To observe the protective effect of α-lipoic acid (α-LA) on oxidative damage of HepG_2 cells induced by cadmium chloride (CdCl_2). Methods In this study, HepG_2 cells as the research object, CdCl 2 induced cell oxidative damage model. The experimental groups were as follows: normal control group, CdCl 2 alone group, α-LA alone group and α-LA + CdCl 2 combined group were cultured in vitro with different concentrations of α-LA (1μM, 5μM, 50μM) The cells were treated with CdCl2 for a final concentration of 25μM. Cell viability was measured by MTT assay. DNA damage was detected by comet assay. The levels of reactive oxygen species (ROS) and malondialdehyde (MDA) . Results Compared with the normal control group, the cell viability (0.814 ± 0.756), the intracellular ROS level (987.18 ± 14.529), the MDA content (1.256 3 ± 0.964) increased and the DNA (4.398 ± 1.068) Severely damaged. Pretreatment with α-LA at different concentrations (1μM, 5μM, 50μM) reduced cell injury induced by CdCl_2 [(0.843 ± 0.658), (0.906 ± 0.469), (0.954 ± 1.163)] and decreased intracellular ROS [(973.40 (0.973 4 ± 0.154), (0.672 9 ± 0.125), (0.534 3 ± 0.156)] and DNA damage [P <0.01] (4.263 ± 0.093), (3.764 ± 0.087), (2.659 ± 0.116)], respectively, and showed a dose-response relationship with α-LA concentration. Conclusion α-LA can antagonize the CdCl2-induced oxidative stress in HepG2 cells and reduce the oxidative damage induced by CdCl2-induced HepG2 cells.