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Article Open Access

Silybin attenuates LPS-induced lung injury in mice by inhibiting NF-κB signaling and NLRP3 activation

  • Authors:
    • Bo Zhang
    • Bing Wang
    • Shuhua Cao
    • Yongqiang Wang
    • Di Wu
  • View Affiliations / Copyright

    Affiliations: Intensive Care Unit, Tianjin Huanhu Hospital, Tianjin Key Laboratory of Cerebral Vascular and Neurodegenerative Diseases, Hexi, Tianjin 300060, P.R. China, Intensive Care Unit, Tianjin First Center Hospital, Tianjin Ιnstitute of Εmergency Μedicine, Nankai, Tianjin 300192, P.R. China
    Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 1111-1118
    |
    Published online on: March 27, 2017
       https://doi.org/10.3892/ijmm.2017.2935
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Abstract

Silybin is one of the main flavonoids produced by milk thistle, which has been used in the treatment of liver diseases. In this study, we examined the protective effects and possible mechanisms of action of silybin in lipopolysaccharide (LPS)‑induced lung injury and inflammation. Pre-treatment of mice with silybin significantly inhibited LPS-induced airway inflammatory cell recruitment, including macrophages, T cells and neutrophils. The production of cytokines, such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in bronchoalveolar fluid and serum was also decreased following treatment with silybin. Elevated cytokine mRNA levels induced by LPS in lung tissue were all suppressed by silybin and lung histological alterations were also improved. In addition, experiments using cells indicated that silybin significantly decreased the mRNA levels and secretion of IL-1β and TNF-α in THP-1 cells. Moreover, the mechanisms responsible for these effects were attributed to the inhibitory effect of silybin on nuclear factor-κB (NF-κB) signaling and NLR family pyrin domain containing 3 (NLRP3) inflammasome activation. The data form our study thus support the utility of silybin as a potential medicine for the treatment of acute lung injury‑associated inflammation and pathological changes. Silybin exerts protective effects against lung injury by regulating NF-κB signaling and the NLRP3 inflammasome activation.
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Copy and paste a formatted citation
Spandidos Publications style
Zhang B, Wang B, Cao S, Wang Y and Wu D: Silybin attenuates LPS-induced lung injury in mice by inhibiting NF-κB signaling and NLRP3 activation. Int J Mol Med 39: 1111-1118, 2017.
APA
Zhang, B., Wang, B., Cao, S., Wang, Y., & Wu, D. (2017). Silybin attenuates LPS-induced lung injury in mice by inhibiting NF-κB signaling and NLRP3 activation. International Journal of Molecular Medicine, 39, 1111-1118. https://doi.org/10.3892/ijmm.2017.2935
MLA
Zhang, B., Wang, B., Cao, S., Wang, Y., Wu, D."Silybin attenuates LPS-induced lung injury in mice by inhibiting NF-κB signaling and NLRP3 activation". International Journal of Molecular Medicine 39.5 (2017): 1111-1118.
Chicago
Zhang, B., Wang, B., Cao, S., Wang, Y., Wu, D."Silybin attenuates LPS-induced lung injury in mice by inhibiting NF-κB signaling and NLRP3 activation". International Journal of Molecular Medicine 39, no. 5 (2017): 1111-1118. https://doi.org/10.3892/ijmm.2017.2935
Copy and paste a formatted citation
x
Spandidos Publications style
Zhang B, Wang B, Cao S, Wang Y and Wu D: Silybin attenuates LPS-induced lung injury in mice by inhibiting NF-κB signaling and NLRP3 activation. Int J Mol Med 39: 1111-1118, 2017.
APA
Zhang, B., Wang, B., Cao, S., Wang, Y., & Wu, D. (2017). Silybin attenuates LPS-induced lung injury in mice by inhibiting NF-κB signaling and NLRP3 activation. International Journal of Molecular Medicine, 39, 1111-1118. https://doi.org/10.3892/ijmm.2017.2935
MLA
Zhang, B., Wang, B., Cao, S., Wang, Y., Wu, D."Silybin attenuates LPS-induced lung injury in mice by inhibiting NF-κB signaling and NLRP3 activation". International Journal of Molecular Medicine 39.5 (2017): 1111-1118.
Chicago
Zhang, B., Wang, B., Cao, S., Wang, Y., Wu, D."Silybin attenuates LPS-induced lung injury in mice by inhibiting NF-κB signaling and NLRP3 activation". International Journal of Molecular Medicine 39, no. 5 (2017): 1111-1118. https://doi.org/10.3892/ijmm.2017.2935
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