title: The inhibitory effect of celecoxib and rosiglitazone on experimental endometriosis.
abstract: OBJECTIVE
  To evaluate the effects of celecoxib and rosiglitazone on the implantation and growth of endometriotic-like lesions in a murine model of endometriosis.
  
  
  METHODS
  Prospective experimental study.
  
  
  METHODS
  Animal research and laboratory facility.
  
  
  METHODS
  Two-month-old female BALB/c mice.
  
  
  METHODS
  Surgically induced endometriosis in female BALB/C mice; 28 days of treatment with celecoxib, rosiglitazone, or their combination; counting, measuring, excising, and fixing lesions.
  
  
  METHODS
  Immunohistochemical examination for proliferating cell nuclear antigen (PCNA), CD31, and CD34 to assess cell proliferation and vascularization, with the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) technique for apoptosis evaluation.
  
  
  RESULTS
  Celecoxib and the combined treatment (celecoxib and rosiglitazone) statistically significantly reduced the mean number of lesions established per mouse, and all treatments diminished the implant volume. In addition, cell proliferation within the implants was statistically significantly reduced, and apoptosis was statistically significantly enhanced by all treatments. Also, we found that all treatments diminished the vascularized area in the lesion.
  
  
  CONCLUSIONS
  These results are promising and reveal that celecoxib and rosiglitazone, combined or separately, have a beneficial effect on overall endometriotic growth.
authors.affiliation: Instituto de Biología y Medicina Experimental (IBYME), CONICET, Ciudad Autónoma de Buenos Aires, Buenos Aires, Argentina. carla.olivares@ibyme.conicet.gov.ar
authors.forename: Carla
authors.initials: C
authors.lastname: Olivares
authors.forename: Analía
authors.initials: A
authors.lastname: Ricci
authors.forename: Mariela
authors.initials: M
authors.lastname: Bilotas
authors.forename: Rosa Inés
authors.initials: RI
authors.lastname: Barañao
authors.forename: Gabriela
authors.initials: G
authors.lastname: Meresman
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D018952:Antigens, CD34 / Q000378:metabolism; D017209:Apoptosis / Q000187:drug effects; D000068579:Celecoxib; D049109:Cell Proliferation / Q000187:drug effects; D052246:Cyclooxygenase 2 Inhibitors / Q000494:pharmacology*; D004195:Disease Models, Animal; D004359:Drug Therapy, Combination; D004715:Endometriosis / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D005260:Female; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D051379:Mice; D008807:Mice, Inbred BALB C; D009389:Neovascularization, Pathologic / Q000517:prevention & control; D047495:PPAR gamma / Q000819:agonists; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000378:metabolism; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D011720:Pyrazoles / Q000494:pharmacology*; D000077154:Rosiglitazone; D013449:Sulfonamides / Q000494:pharmacology*; D045162:Thiazolidinediones / Q000494:pharmacology*; D013997:Time Factors; D014599:Uterus / Q000637:transplantation
chemical_list: D018952:Antigens, CD34; D052246:Cyclooxygenase 2 Inhibitors; D047495:PPAR gamma; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D018809:Proliferating Cell Nuclear Antigen; D011720:Pyrazoles; D013449:Sulfonamides; D045162:Thiazolidinediones; D000077154:Rosiglitazone; D000068579:Celecoxib