Influence of different concentrations of uric acid on oxidative stress in steatosis hepatocytes

Cheng,Shi; Yang,Yan; Zhou,Yong; Xiang,Wei; Yao,Hua; Ma,Ling

doi:10.3892/etm.2018.5855

Influence of different concentrations of uric acid on oxidative stress in steatosis hepatocytes

Authors:
- Shi Cheng
- Yan Yang
- Yong Zhou
- Wei Xiang
- Hua Yao
- Ling Ma
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Affiliations: Department of Nutrition and Food Hygiene, School of Public Health, Xinjiang Medical University, Urumqi, Xinjiang 830011, P.R. China, Department of Child Healthcare, People's Hospital (Children's Hospital) North Hospital, Urumqi, Xinjiang 830011, P.R. China, Department of Biology, School of Basic Medicine, Xinjiang Medical University, Urumqi, Xinjiang 830011, P.R. China, Health Management Department, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang 830054, P.R. China
Published online on: February 12, 2018 https://doi.org/10.3892/etm.2018.5855
Pages: 3659-3665

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Abstract

The development of nonalcoholic fatty liver disease (NAFLD) is caused by the steatosis of hepatocytes, which induces oxidative stress (OS). Thus, OS has an important role in the development of NAFLD. In the present study, the L‑02 hepatocyte cell line was used to develop a steatosis cell model. The best model was determined using an MTT assay and the triglyceride levels. Model cells were treated with high concentrations of uric acid (UA; 0, 5, 10, 20 and 30 mg/dl) for 24, 48, 72 and 96 h. Indicators of oxidation were then measured, which included total superoxide dismutase (SOD), malonaldehyde (MDA) and reduced glutathione (GSH), and the transcriptional and translational levels of SOD1 and γ‑glutamate‑cysteine ligase (γ‑GCLC) were also determined. In addition, the intracellular levels of aspartate aminotransferase and alanine aminotransferase (ALT) were detected. The activity of SOD1 decreased over time and the result was supported by the results of western blotting. The transcriptional levels of SOD1 in model cells was significantly higher than untreated cells at 48 h. With the decreased levels of SOD1 and GSH, MDA increased in a time‑dependent manner. The content of GSH decreased with time as well, which was also reflected in the results of western blotting. The transcriptional levels of γ‑GCLC in all UA‑treated groups were lower when compared with those observed in the model group. The activity of ALT tended to increase, depending on the duration of treatment. Treatment with 5 and 10 mg/dl UA had an antioxidative effect on the model cells, and 30 mg/dl UA treatment for 48 h increased OS in the cells.

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