Sodium butyrate protects against oxidative stress in HepG2 cells through modulating Nrf2 pathway and mitochondrial function

Xingan Xing; Zheshu Jiang; Xue Tang; Panpan Wang; Yingrui Li; Yongjuan Sun; Guowei Le; Sixiang Zou

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Sodium butyrate protects against oxidative stress in HepG2 cells through modulating Nrf2 pathway and mitochondrial function

Xingan Xing ^[1] ; Zheshu Jiang ^[3] ; Xue Tang ^[1] ; Panpan Wang ^[1] ; Yingrui Li ^[1] ; Yongjuan Sun ^[1] ; Guowei Le ^[1] ; Sixiang Zou ^[2]
1. [1] Jiangnan University
  
  Jiangnan University
  
  China
2. [2] Nanjing Agricultural University
  
  Nanjing Agricultural University
  
  China
3. [3] Wuxi No.1 Senior High School, China
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Localización: Journal of physiology and biochemistry, ISSN-e 1877-8755, ISSN 1138-7548, Vol. 73, Nº. 3 (August 2017), 2017 (Ejemplar dedicado a: CTPIOD meeting (Contribution To Progress in Obesity and Diabetes Research) 2016), págs. 405-414
Idioma: inglés
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Resumen
- Sodium butyrate (NaBu) is a by-product of microbial fermentation of dietary fiber in the gastrointestinal tract and has been shown to increase the activity of antioxidant enzymes, such as catalase or heme oxidase-1, in vivo. However, the mechanism of this effect is still unclear. This study investigated the antioxidant effect of NaBu on HepG2 cells under H2O2-induced oxidative stress. NaBu (0.3 mM) attenuated cell death and accumulation of reactive oxygen species and improved multiple antioxidant parameters in H2O2-injured HepG2 cells. NaBu inhibited glycogen synthase kinase-3 beta (GSK-3β) by increasing the p-GSK-3β (Ser9) level and promoted nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2), which increased the expression of downstream antioxidant enzymes. Together with promotion of peroxisome proliferator-activated receptor gamma coactivator 1-alpha and mitochondrial DNA copy number, NaBu modulated energy metabolism and mitochondrial function, decreasing glycolysis, increasing β-oxidation, and enhancing the tricarboxylic acid cycle and oxidative phosphorylation. NaBu increased mitochondrial manganese-superoxide dismutase and glutathione peroxidase activity. In conclusion, NaBu protected HepG2 cells against oxidative stress by modulating Nrf2 pathway activity and mitochondrial function.