Open Access

Emodin suppresses silica-induced lung fibrosis by promoting Sirt1 signaling via direct contact

  • Authors:
    • Tian Yang
    • Jinyuan Wang
    • Yamei Pang
    • Xiaomin Dang
    • Hui Ren
    • Ya Liu
    • Mingwei Chen
    • Dong Shang
  • View Affiliations

  • Published online on: October 12, 2016     https://doi.org/10.3892/mmr.2016.5838
  • Pages: 4643-4649
  • Copyright: © Yang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Pulmonary silicosis is characterized by lung fibrosis, which leads to impairment of pulmonary function; the specific mechanism remains to be fully elucidated Emodin shows antifibrotic effects in several organs with fibrosis, however, it has not been investigated in pulmonary silicosis. In the present study, the possible mechanism of lung fibrosis and the antifibrotic effect of emodin in silica inhalation‑induced lung fibrosis were investigated. Pulmonary silica particle inhalation was used to induce lung fibrosis in mice. Emodin and or the sirtuin 1 (Sirt1) inhibitor, nicotinamide, were used to treat the modeled animals. Pulmonary function was assessed using an occlusion method. The deposition of collagen I and α‑smooth muscle actin (SMA) in the lung tissue were detected using fluorescence staining; transforming growth factor‑β1 (TGF‑β1) in the bronchoalveolar lavage fluid (BALF) was examined using an enzyme‑linked immunosorbent assay; TGF-β1/Sirt1/small mothers against decapentaplegic (Smad) signaling activation in lung tissue was also examined. The molecular contacts between emodin were evaluated using liquid chromatography‑mass spectrometry analysis. The deposition of collagen I and α‑SMA in lung tissues were found to be elevated following silica exposure, however, this was relieved by emodin treatment. The pulmonary function of the animals was impaired by silica inhalation, and this was improved by emodin administration. However, the therapeutic effects of emodin on lung fibrosis were impaired by nicotinamide administration. The levels of TGF‑β1 in the BALF and lung tissue were elevated by silica inhalation, however, they were not affected by either emodin or nicotinamide treatment. Additionally, emodin was found to increase the expression level of Sirt1, which decreased the level of deacetylated Smad3 to attenuate collagen deposition. Furthermore, the data suggested that there was direct binding between emodin and Sirt1. Sirt1‑regulated TGF‑β1/Smad signaling was involved in silica inhalation‑induced lung fibrosis. Emodin attenuated this lung fibrosis to improve pulmonary function by targeting Sirt1, which regulated TGF-β1/Smad fibrotic signaling.
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November-2016
Volume 14 Issue 5

Print ISSN: 1791-2997
Online ISSN:1791-3004

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Copy and paste a formatted citation
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Spandidos Publications style
Yang T, Wang J, Pang Y, Dang X, Ren H, Liu Y, Chen M and Shang D: Emodin suppresses silica-induced lung fibrosis by promoting Sirt1 signaling via direct contact. Mol Med Rep 14: 4643-4649, 2016
APA
Yang, T., Wang, J., Pang, Y., Dang, X., Ren, H., Liu, Y. ... Shang, D. (2016). Emodin suppresses silica-induced lung fibrosis by promoting Sirt1 signaling via direct contact. Molecular Medicine Reports, 14, 4643-4649. https://doi.org/10.3892/mmr.2016.5838
MLA
Yang, T., Wang, J., Pang, Y., Dang, X., Ren, H., Liu, Y., Chen, M., Shang, D."Emodin suppresses silica-induced lung fibrosis by promoting Sirt1 signaling via direct contact". Molecular Medicine Reports 14.5 (2016): 4643-4649.
Chicago
Yang, T., Wang, J., Pang, Y., Dang, X., Ren, H., Liu, Y., Chen, M., Shang, D."Emodin suppresses silica-induced lung fibrosis by promoting Sirt1 signaling via direct contact". Molecular Medicine Reports 14, no. 5 (2016): 4643-4649. https://doi.org/10.3892/mmr.2016.5838