Nonsteroidal antiinflammatory drugs differentially suppress endometriosis in a murine model

被引:93
作者
Efstathiou, JA
Sampson, DA
Levine, Z
Rohan, RM
Zurakowski, D
Folkman, J
D'Amato, RJ
Rupnick, MA
机构
[1] Childrens Hosp, Vasc Biol Program, Boston, MA 02115 USA
[2] Childrens Hosp, Dept Surg, Boston, MA 02115 USA
[3] Childrens Hosp, Dept Orthoped Surg & Biostat, Boston, MA 02115 USA
[4] Brigham & Womens Hosp, Dept Obstet & Gynecol, Boston, MA USA
[5] Brigham & Womens Hosp, Dept Cardiol, Boston, MA USA
[6] Harvard Univ, Sch Med, Dept Ophthalmol, Boston, MA USA
[7] MIT, Dept Chem Engn, Cambridge, MA USA
关键词
endometriosis; angiogenesis; neovascularization; nonsteroidal; antiiflammatory drugs; NSAIDs;
D O I
10.1016/j.fertnstert.2004.06.058
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
Objective: To determine whether nonsteroidal antiinflammatory drugs (NSAIDs) affect the establishment and progression of endometriotic lesions in a murine model. Design: Pharmacologic intervention in a surgically induced murine model of abdominal/peritoneal endometriosis. Setting: Animal research facility. Patient(s): 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. Main Outcome Measure(s): Establishment, growth, and total burden of endometriotic lesions. Result(s): 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. Conclusion(s): 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. (C)2005 by American Society for Reproductive Medicine.
引用
收藏
页码:171 / 181
页数:11
相关论文
共 42 条
[1]  
Barbieri RL, 1998, J REPROD MED, V43, P287
[2]   DETERMINING STAGE OF ESTROUS-CYCLE IN MOUSE BY APPEARANCE OF VAGINA [J].
CHAMPLIN, AK ;
DORR, DL ;
GATES, AH .
BIOLOGY OF REPRODUCTION, 1973, 8 (04) :491-&
[3]   The epidemiology of endometriosis [J].
Cramer, DW ;
Missmer, SA .
ENDOMETRIOSIS: EMERGING RESEARCH AND INTERVENTION STRATEGIES, 2002, 955 :11-22
[4]  
CRAMER DW, 2002, ANN NY ACAD SCI, V955, P396
[5]   INDUCTION OF ENDOMETRIOSIS IN MICE - A NEW MODEL SENSITIVE TO ESTROGEN [J].
CUMMINGS, AM ;
METCALF, JL .
REPRODUCTIVE TOXICOLOGY, 1995, 9 (03) :233-238
[6]   Therapeutic effect of angiostatin gene transfer in a murine model of endometriosis [J].
Dabrosin, C ;
Gyorffy, S ;
Margetts, P ;
Ross, C ;
Gauldie, J .
AMERICAN JOURNAL OF PATHOLOGY, 2002, 161 (03) :909-918
[7]  
Dargenio R, 1992, Acta Eur Fertil, V23, P85
[8]   Morphologic characteristics of endometriosis in the mouse model: application to toxicology [J].
Foster, WG ;
Ruka, MP ;
Gareau, P ;
Foster, RA ;
Janzen, EG ;
Yang, JZ .
CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY, 1997, 75 (10-11) :1188-1196
[9]   Peritoneal environment, cytokines and angiogenesis in the pathophysiology of endometriosis [J].
Gazvani, R ;
Templeton, A .
REPRODUCTION, 2002, 123 (02) :217-226
[10]  
GOLAN A, 1986, FERTIL STERIL, V46, P954