Aquaporin Changes in Compound 48/80 Induced Inflammatory Sublaryngeal Edema in Rat

  • Yongxin Liu
    Affiliations
    Department of Anatomy, China Medical University, Shenyang, China

    Department of Otolaryngology Head and Neck Surgery, The First Hospital of Liaoning Medical College, Jinzhou, China
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  • Huanjiu Xi
    Correspondence
    Address correspondence and reprint requests to Huanjiu Xi, Department of Anatomy, China Medical University, #92, Beier Road, Heping District, Shenyang 110001, China.
    Affiliations
    Department of Anatomy, China Medical University, Shenyang, China

    Anthropology Institute, Liaoning Medical College, Jinzhou, China
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  • Weiwei Xing
    Affiliations
    Department of Otolaryngology Head and Neck Surgery, The First Hospital of Liaoning Medical College, Jinzhou, China
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  • Jingcheng Gu
    Affiliations
    Department of Otolaryngology Head and Neck Surgery, The First Hospital of Liaoning Medical College, Jinzhou, China
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      Summary

      Objectives/Hypothesis

      Laryngeal edema is a common clinical condition. However, the underlying molecular mechanisms remain elusive. Aquaporins (AQPs) are small integral plasma membrane proteins that transport water across the plasma membrane. In this study, we explore the relationship between inflammatory laryngeal edema induced by compound 48/80 and the expression of AQPs.

      Study Design

      Prospective, controlled, experimental animal study.

      Methods

      Healthy adult male SD rats were injected with either sterile water, compound 48/80 (2 mg/kg), or compound 48/80 plus dexamethasone (3 mg/kg) via the tail vein. The larynxes were harvested 10, 30 minutes, and 1 hour after the injection for the measurement of sublaryngeal water content and histological and molecular evaluations.

      Results

      Ten and 30 minutes after the compound 48/80 injection compared with the sterile water injection control groups, the water content in subglottic larynx increased significantly and the tissues were markedly swollen accompanied with inflammatory cell infiltration. AQP1 and AQP5 mRNA decreased significantly. One hour after the compound 48/80 injection, the edema was diminished, but the inflammatory cell infiltration remained. AQP1 was elevated but AQP5 was still lower than controls. Dexamethasone did not significantly reduce laryngeal edema, but significantly reduced inflammatory cells infiltration induced by compound 48/80 injection. Dexamethasone increased the AQP5 level but not AQP1.

      Conclusions

      AQP1 and AQP5 might play key roles in inflammatory subglottic edema caused by compound 48/80 in rats. AQP1 and AQP5 might be useful molecular targets of clinical treatment of inflammatory laryngeal edema.

      Key Words

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