title: Nonsteroidal antiinflammatory drugs differentially suppress endometriosis in a murine model.
abstract: OBJECTIVE
  To determine whether nonsteroidal antiinflammatory drugs (NSAIDs) affect the establishment and progression of endometriotic lesions in a murine model.
  
  
  METHODS
  Pharmacologic intervention in a surgically induced murine model of abdominal/peritoneal endometriosis.
  
  
  METHODS
  Animal research facility.
  
  
  METHODS
  Eight-week-old, female C57BL/6 mice.
  
  
  METHODS
  After implantation of autologous endometrium, mice were randomized into groups and treated with one of several NSAIDs or the vehicle-matched control for 4 weeks.
  
  
  METHODS
  Establishment, growth, and total burden of endometriotic lesions.
  
  
  RESULTS
  The NSAIDs differentially inhibited lesion establishment and growth, resulting in significantly reduced disease burden. Compared with controls (5.7 +/- 2.3 mm(2)), lesion burden was reduced by celecoxib (1.3 +/- 1.2 mm(2)), indomethacin (1.4 +/- 1.4 mm(2)), naproxen (2.7 +/- 1.2 mm(2)), sulindac (3.1 +/- 1.5 mm(2)), rofecoxib (3.4 +/- 3.0 mm(2)), and ibuprofen (4.1 +/- 1.4 mm(2)). In contrast, aspirin (5.9 +/- 1.2 mm(2)) had no statistically significant effect. Uninterrupted estrus cycling was confirmed by vaginal exams and smears in celecoxib-treated mice.
  
  
  CONCLUSIONS
  Chronic administration of certain NSAIDs limits the progression of endometriosis in this murine model. The data suggest that NSAID selection in the treatment of endometriosis should be extended beyond pain management to maximize the inhibitory effect on disease burden.
authors.affiliation: Department of Surgery, Children's Hospital, Boston, Massachusetts 02115-5737, USA.
authors.forename: Jason A
authors.initials: JA
authors.lastname: Efstathiou
authors.forename: David A
authors.initials: DA
authors.lastname: Sampson
authors.forename: Zalman
authors.initials: Z
authors.lastname: Levine
authors.forename: Richard M
authors.initials: RM
authors.lastname: Rohan
authors.forename: David
authors.initials: D
authors.lastname: Zurakowski
authors.forename: Judah
authors.initials: J
authors.lastname: Folkman
authors.forename: Robert J
authors.initials: RJ
authors.lastname: D'Amato
authors.forename: Maria A
authors.initials: MA
authors.lastname: Rupnick
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use*; D000068579:Celecoxib; D016861:Cyclooxygenase Inhibitors / Q000627:therapeutic use*; D004195:Disease Models, Animal; D004715:Endometriosis / Q000188:drug therapy* / Q000473:pathology; D005260:Female; D006801:Humans; D051379:Mice; D008810:Mice, Inbred C57BL; D011720:Pyrazoles / Q000627:therapeutic use*; D013449:Sulfonamides / Q000627:therapeutic use*
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D016861:Cyclooxygenase Inhibitors; D011720:Pyrazoles; D013449:Sulfonamides; D000068579:Celecoxib