Protective effects of dimethylthiourea against hydrogen peroxide-induced oxidative stress in hepatic L02 cell

被引:0
|
作者
Liu, Yipin [1 ]
Sun, Xuehui [2 ]
Jiang, Weiwei [1 ]
Cao, Xiaoling [1 ]
机构
[1] Binzhou Med Univ, Yantai Affiliated Hosp, Dept Gastroenterol, 717 Jinbu St, Yantai 264100, Peoples R China
[2] Qingdao Univ, Affiliated Yantai Yuhuangding Hosp, Dept Rheumatol, Yantai 264000, Peoples R China
关键词
Apoptosis; dimethylthiourea; hepatic L02 cell; hepatoprotective; oxidative stress; H2O2-INDUCED APOPTOSIS; LIVER-INJURY; MECHANISMS; ACTIVATION; RADICALS; OXYGEN;
D O I
暂无
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Context: Oxidative stress and mitochondrial dysfunction are hypothesized to contribute to the pathogenesis of chronic cholestatic liver diseases. Objective: This study aims to explore the effects of dimethylthiourea (DMTU) preconditioning on human hepatocytes L02 cells against hydrogen peroxide (H2O2) -induced oxidative stress. Methods: Preconditioned or non-preconditioned human hepatic L02 cells were exposed to H2O2 with certain concentration and the cell viability was detected by MTT assay. Lactate dehydrogenase (LDH), superoxide dismutase (SOD), glutathione (GSH-Px), and malondialdehyde (MDA) levels were evaluated with corresponding ELISA kits. Caspase-3 activity was determined with Caspase-Glo 3/7 assay kit. Bax/Bcl-2 ratio was measured by Western blot. Results: DMTU preconditioning could significantly ameliorate L02 cells viability loss, promote the decreased SOD and GSH-Px levels and attenuate the cascade of MDA level and LDH leakage induced by H2O2. DMTU administration could also reinforce the activity of caspase-3 and increase the Bax/Bcl-2 ratio to inhibit apoptosis and improve the L02 cells activity. Conclusions: These results indicated that DMTU could protect the hepatic L02 cells against H2O2-induced liver injury by alleviating oxidative stress and apoptosis process, and DMTU might be potential hepatoprotective medicine.
引用
收藏
页码:5114 / 5121
页数:8
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