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Article Open Access

Fisetin administration improves LPS-induced acute otitis media in mouse in vivo

  • Authors:
    • Peng Li
    • Dan Chen
    • Yang Huang
  • View Affiliations / Copyright

    Affiliations: Department of Otorhinolaryngology, The Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510630, P.R. China, Department of Otolaryngology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510630, P.R. China, Department of Otolaryngology, The First People's Hospital of Yunnan Province, Xishan, Kunming 650032, P.R. China
    Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 237-247
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    Published online on: March 22, 2018
       https://doi.org/10.3892/ijmm.2018.3585
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Abstract

Acute otitis media is one of the most common infectious diseases worldwide in spite of the widespread vaccination. The present study was conducted to explore the effects of fisetin on mouse acute otitis media models. The animal models were established by lipopolysaccharide (LPS) injection into the middle ear of mice via the tympanic membrane. Fisetin was administered to mice for ten days through intragastric administration immediate after LPS application. Hematoxylin and eosin (H&E) staining was performed and the pro-inflammatory cytokines, including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), IL-6 and VEGF, were measured through enzyme-linked immunosorbent assay (ELISA) method and RT-qPCR analysis. Toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) signaling pathway was detected by immunoblotting assays. Reactive oxygen species (ROS) generated levels were determined through assessment of anti-oxidants, and TXNIP/MAPKs signaling pathways were explored to reveal the possible molecular mechanism for acute otitis media progression and the function of fisetin. Fisetin reduced mucosal thickness caused by LPS. In fisetin-treated animals, pro-inflammatory cytokine release was downregulated accompanied with TLR4/NF-κB inactivation. ROS production was significantly decreased in comparison to the LPS-treated group. The TXNIP/MAPKs signaling pathway was inactivated for fisetin treatment in LPS-induced mice with acute otitis media. The above results indicated that fisetin improved acute otitis media through inflammation and ROS suppression via inactivating TLR4/NF-κB and TXNIP/MAPKs signaling pathways.
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Copy and paste a formatted citation
Spandidos Publications style
Li P, Chen D and Huang Y: Fisetin administration improves LPS-induced acute otitis media in mouse in vivo. Int J Mol Med 42: 237-247, 2018.
APA
Li, P., Chen, D., & Huang, Y. (2018). Fisetin administration improves LPS-induced acute otitis media in mouse in vivo. International Journal of Molecular Medicine, 42, 237-247. https://doi.org/10.3892/ijmm.2018.3585
MLA
Li, P., Chen, D., Huang, Y."Fisetin administration improves LPS-induced acute otitis media in mouse in vivo". International Journal of Molecular Medicine 42.1 (2018): 237-247.
Chicago
Li, P., Chen, D., Huang, Y."Fisetin administration improves LPS-induced acute otitis media in mouse in vivo". International Journal of Molecular Medicine 42, no. 1 (2018): 237-247. https://doi.org/10.3892/ijmm.2018.3585
Copy and paste a formatted citation
x
Spandidos Publications style
Li P, Chen D and Huang Y: Fisetin administration improves LPS-induced acute otitis media in mouse in vivo. Int J Mol Med 42: 237-247, 2018.
APA
Li, P., Chen, D., & Huang, Y. (2018). Fisetin administration improves LPS-induced acute otitis media in mouse in vivo. International Journal of Molecular Medicine, 42, 237-247. https://doi.org/10.3892/ijmm.2018.3585
MLA
Li, P., Chen, D., Huang, Y."Fisetin administration improves LPS-induced acute otitis media in mouse in vivo". International Journal of Molecular Medicine 42.1 (2018): 237-247.
Chicago
Li, P., Chen, D., Huang, Y."Fisetin administration improves LPS-induced acute otitis media in mouse in vivo". International Journal of Molecular Medicine 42, no. 1 (2018): 237-247. https://doi.org/10.3892/ijmm.2018.3585
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