title: The selective COX-2 inhibitor Etoricoxib reduces acute inflammatory markers in a model of neurogenic laryngitis but loses its efficacy with prolonged treatment.
abstract: OBJECTIVE
  A randomised experimental study was used to evaluate the therapeutic effect of a selective cyclooxygenase-2 (COX-2) inhibitor in neurogenic laryngitis.
  
  
  METHODS
  Male Wistar Han rats were subjected to the nasogastric intubation model (NGI) of laryngitis for 1 and 2 weeks. The NGI animals were divided into three groups: (1) treated with COX-2 inhibitor Etoricoxib, (2) vehicle and (3) non-intubated animals. A fourth group of animals was submitted to NGI only. Laryngeal sections were immunostained for substance P (SP) and calcitonin gene-related peptide (CGRP) fibre-immunoreactivity (IR) and quantification of COX-2 positive cells through stereological analysis. The expression of COX-2, interleukins IL-1beta, IL-6, IL-10 and tumour necrosis factor-alpha (TNF-alpha) was determined by quantitative real time QRT-PCR.
  
  
  METHODS
  Etoricoxib (6 mg/kg/day) was prepared in 0.9% sterile saline with 5% glucose (vehicle) and administered daily during 1 or 2 weeks.
  
  
  RESULTS
  Treatment for 1 week with Etoricoxib attenuated the CGRP-IR fibre depletion, the COX-2-IR increased cell number and the TNF-alpha and COX-2 mRNA increased levels induced by NGI. Two weeks of treatment had no beneficial effect.
  
  
  CONCLUSIONS
  Etoricoxib is effective in neurogenic laryngitis for limited periods of administration, indicating that selective COX-2 inhibitors should be evaluated in the future.
authors.affiliation: Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Braga, Portugal.
authors.forename: Manuel
authors.initials: M
authors.lastname: Lima-Rodrigues
authors.forename: Nuno
authors.initials: N
authors.lastname: Lamas
authors.forename: Ana
authors.initials: A
authors.lastname: Valle-Fernandes
authors.forename: Andrea
authors.initials: A
authors.lastname: Cruz
authors.forename: Artur
authors.initials: A
authors.lastname: Vieira
authors.forename: Pedro
authors.initials: P
authors.lastname: Oliveira
authors.forename: Jorge
authors.initials: J
authors.lastname: Pedrosa
authors.forename: António G
authors.initials: AG
authors.lastname: Castro
authors.forename: Rui M
authors.initials: RM
authors.lastname: Reis
authors.forename: Fátima
authors.initials: F
authors.lastname: Baltazar
authors.forename: Armando
authors.initials: A
authors.lastname: Almeida
mesh_terms: D000818:Animals; D015740:Calcitonin Gene-Related Peptide / Q000032:analysis; D051546:Cyclooxygenase 2 / Q000032:analysis; D052246:Cyclooxygenase 2 Inhibitors / Q000627:therapeutic use*; D004195:Disease Models, Animal; D000077613:Etoricoxib; D016753:Interleukin-10 / Q000032:analysis; D053583:Interleukin-1beta / Q000032:analysis; D015850:Interleukin-6 / Q000032:analysis; D007827:Laryngitis / Q000188:drug therapy* / Q000276:immunology; D008297:Male; D011725:Pyridines / Q000627:therapeutic use*; D051381:Rats; D017208:Rats, Wistar; D013373:Substance P / Q000032:analysis; D013450:Sulfones / Q000627:therapeutic use*; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D052246:Cyclooxygenase 2 Inhibitors; D053583:Interleukin-1beta; D015850:Interleukin-6; D011725:Pyridines; D013450:Sulfones; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D013373:Substance P; D051546:Cyclooxygenase 2; D015740:Calcitonin Gene-Related Peptide; D000077613:Etoricoxib