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

Abstract

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. Prospective, controlled, experimental animal study. 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. 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. 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.