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Sulforaphane increases Nrf2 expression and protects alveolar epithelial cells against injury caused by cigarette smoke extract

  • Authors:
    • Zongxian Jiao
    • Jiachen Chang
    • Jing Li
    • Dengmei Nie
    • Huijuan Cui
    • Dongfang Guo
  • View Affiliations / Copyright

    Affiliations: Research Institute of Pathology, School of Basic Medical Sciences, Lanzhou University, Lanzhou, Gansu 730000, P.R. China
    Copyright: © Jiao et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 1241-1247
    |
    Published online on: June 6, 2017
       https://doi.org/10.3892/mmr.2017.6700
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Abstract

Cigarette smoking is a primary risk factor for chronic obstructive pulmonary disease (COPD), as it damages epithelial cells through a variety of mechanisms. Sulforaphane (SFN) is an antioxidant agent, which exerts protective effects against cell damage by activating the nuclear factor erythroid 2 like 2 (NFE2L2; Nrf2). The present study was undertaken to investigate the effects and underlying mechanisms of SFN in preventing cigarette smoke extract (CSE)‑induced oxidative damage to RLE‑6TN rat lung epithelial cells. MTT assay was used to determine the cytotoxicity of SFN and CSE. The effect of SFN and CSE on cell cycle progression, apoptosis and intracellular reactive oxygen species (ROS) levels were analyzed using flow cytometry. Reverse transcription‑quantitative polymerase chain reaction and western blotting were used to quantify mRNA and protein expression levels of Nrf2 respectively. SFN protected RLE‑6TN cells from oxidative damage, potentially via increasing Nrf2 expression and reducing ROS levels. In addition, SFN attenuated G1 phase cell cycle arrest and abrogated apoptosis. Therefore, SFN protected alveolar epithelial cells against CSE‑induced oxidative injury by upregulating Nrf2 expression. The results of the present study may provide theoretical support for the clinical use of SFN in patients with COPD.
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Copy and paste a formatted citation
Spandidos Publications style
Jiao Z, Chang J, Li J, Nie D, Cui H and Guo D: Sulforaphane increases Nrf2 expression and protects alveolar epithelial cells against injury caused by cigarette smoke extract. Mol Med Rep 16: 1241-1247, 2017.
APA
Jiao, Z., Chang, J., Li, J., Nie, D., Cui, H., & Guo, D. (2017). Sulforaphane increases Nrf2 expression and protects alveolar epithelial cells against injury caused by cigarette smoke extract. Molecular Medicine Reports, 16, 1241-1247. https://doi.org/10.3892/mmr.2017.6700
MLA
Jiao, Z., Chang, J., Li, J., Nie, D., Cui, H., Guo, D."Sulforaphane increases Nrf2 expression and protects alveolar epithelial cells against injury caused by cigarette smoke extract". Molecular Medicine Reports 16.2 (2017): 1241-1247.
Chicago
Jiao, Z., Chang, J., Li, J., Nie, D., Cui, H., Guo, D."Sulforaphane increases Nrf2 expression and protects alveolar epithelial cells against injury caused by cigarette smoke extract". Molecular Medicine Reports 16, no. 2 (2017): 1241-1247. https://doi.org/10.3892/mmr.2017.6700
Copy and paste a formatted citation
x
Spandidos Publications style
Jiao Z, Chang J, Li J, Nie D, Cui H and Guo D: Sulforaphane increases Nrf2 expression and protects alveolar epithelial cells against injury caused by cigarette smoke extract. Mol Med Rep 16: 1241-1247, 2017.
APA
Jiao, Z., Chang, J., Li, J., Nie, D., Cui, H., & Guo, D. (2017). Sulforaphane increases Nrf2 expression and protects alveolar epithelial cells against injury caused by cigarette smoke extract. Molecular Medicine Reports, 16, 1241-1247. https://doi.org/10.3892/mmr.2017.6700
MLA
Jiao, Z., Chang, J., Li, J., Nie, D., Cui, H., Guo, D."Sulforaphane increases Nrf2 expression and protects alveolar epithelial cells against injury caused by cigarette smoke extract". Molecular Medicine Reports 16.2 (2017): 1241-1247.
Chicago
Jiao, Z., Chang, J., Li, J., Nie, D., Cui, H., Guo, D."Sulforaphane increases Nrf2 expression and protects alveolar epithelial cells against injury caused by cigarette smoke extract". Molecular Medicine Reports 16, no. 2 (2017): 1241-1247. https://doi.org/10.3892/mmr.2017.6700
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