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Article

SIRT1‑mediated regulation of oxidative stress induced by Pseudomonas aeruginosa lipopolysaccharides in human alveolar epithelial cells

  • Authors:
    • Xiaoli Liu
    • Tuo Yang
    • Tieying Sun
    • Kuiqing Shao
  • View Affiliations / Copyright

    Affiliations: Department of Respiratory Medicine, Beijing Shijitan Hospital, Capital Medical University, Beijing 100038, P.R. China, Department of Neurology, University of Pittsburgh, Pittsburgh, PA 15260, USA, Department of Respiratory and Critical Care Medicine, Beijing Hospital Ministry of Health, Beijing 100730, P.R. China, Department of Urinary Surgery, Xiyuan Hospital of China Academy of Chinese Medical Sciences, Beijing 100091, P.R. China
  • Pages: 813-818
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    Published online on: December 14, 2016
       https://doi.org/10.3892/mmr.2016.6045
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Abstract

Sirtuin1 (SIRT1) is an NAD+‑dependent deacetylase that exhibits multiple biological functions, including cell differentiation inhibition, transcription regulation, cell cycle regulation and anti‑apoptosis. Lipopolysaccharides (LPS) are crucial virulence factors produced by Pseudomonas aeruginosa and serve an important role in adjusting the interactions between the host and the pathogen. However, the effect of SIRT1 in the regulation of LPS‑induced A459 human alveolar epithelial cells (AECs) oxidative stress remains unclear. The cellular reactive oxygen species (ROS) production was examined in A549 cells that were supplemented with LPS. Relative cell signaling pathway proteins were further investigated by western blot analysis. It was identified that LPS downregulated SIRT1 expression, however, upregulated ROS generation, which was associated with the increase of nuclear factor (NF)‑κB and acetyl‑NF‑κB. Activation of SIRT1 by resveratrol significantly reversed the effects of LPS on A549 cells. By contrast, inhibition of SIRT1 by nicotinamide had the opposite effects that enhance cell ROS production. Thus, the results indicated that SIRT1 serves an important role in the regulation of oxidative stress induced by LPS in human AECs.
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Copy and paste a formatted citation
Spandidos Publications style
Liu X, Yang T, Sun T and Shao K: SIRT1‑mediated regulation of oxidative stress induced by Pseudomonas aeruginosa lipopolysaccharides in human alveolar epithelial cells. Mol Med Rep 15: 813-818, 2017.
APA
Liu, X., Yang, T., Sun, T., & Shao, K. (2017). SIRT1‑mediated regulation of oxidative stress induced by Pseudomonas aeruginosa lipopolysaccharides in human alveolar epithelial cells. Molecular Medicine Reports, 15, 813-818. https://doi.org/10.3892/mmr.2016.6045
MLA
Liu, X., Yang, T., Sun, T., Shao, K."SIRT1‑mediated regulation of oxidative stress induced by Pseudomonas aeruginosa lipopolysaccharides in human alveolar epithelial cells". Molecular Medicine Reports 15.2 (2017): 813-818.
Chicago
Liu, X., Yang, T., Sun, T., Shao, K."SIRT1‑mediated regulation of oxidative stress induced by Pseudomonas aeruginosa lipopolysaccharides in human alveolar epithelial cells". Molecular Medicine Reports 15, no. 2 (2017): 813-818. https://doi.org/10.3892/mmr.2016.6045
Copy and paste a formatted citation
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Spandidos Publications style
Liu X, Yang T, Sun T and Shao K: SIRT1‑mediated regulation of oxidative stress induced by Pseudomonas aeruginosa lipopolysaccharides in human alveolar epithelial cells. Mol Med Rep 15: 813-818, 2017.
APA
Liu, X., Yang, T., Sun, T., & Shao, K. (2017). SIRT1‑mediated regulation of oxidative stress induced by Pseudomonas aeruginosa lipopolysaccharides in human alveolar epithelial cells. Molecular Medicine Reports, 15, 813-818. https://doi.org/10.3892/mmr.2016.6045
MLA
Liu, X., Yang, T., Sun, T., Shao, K."SIRT1‑mediated regulation of oxidative stress induced by Pseudomonas aeruginosa lipopolysaccharides in human alveolar epithelial cells". Molecular Medicine Reports 15.2 (2017): 813-818.
Chicago
Liu, X., Yang, T., Sun, T., Shao, K."SIRT1‑mediated regulation of oxidative stress induced by Pseudomonas aeruginosa lipopolysaccharides in human alveolar epithelial cells". Molecular Medicine Reports 15, no. 2 (2017): 813-818. https://doi.org/10.3892/mmr.2016.6045
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