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Journal of the Society for Gynecologic Investigation, Vol. 13, No. 1, 58-62 (2006)
DOI: 10.1016/j.jsgi.2005.10.002

Effect of Peroxisome Proliferator—Activated Receptor-{gamma} Agonist Rosiglitazone on the Induction of Endometriosis in an Experimental Rat Model

Fazli Demirturk, MD

Department of Obstetrics and Gynecology, Gaziosmanpasa University, Tokat, Turkey; Government of Health Ankara Diskapi Education and Research Hospital, Third Internal Medicine Clinic, Ankara, Turkey; Department of Pathology, Gaziosmanpasa University, Tokat, Turkey

Hakan Aytan, MD

Department of Obstetrics and Gynecology, Gaziosmanpasa University, Tokat, Turkey; Government of Health Ankara Diskapi Education and Research Hospital, Third Internal Medicine Clinic, Ankara, Turkey; Department of Pathology, Gaziosmanpasa University, Tokat, Turkeyv drhakanaytan{at}hotmail.com

Ahmet C. Caliskan, MD

Pelin Aytan, MD

Dogan R. Koseoglu, MD

Department of Obstetrics and Gynecology, Gaziosmanpasa University, Tokat, Turkey; Government of Health Ankara Diskapi Education and Research Hospital, Third Internal Medicine Clinic, Ankara, Turkey; Department of Pathology, Gaziosmanpasa University, Tokat, Turkey

Objective: To assess the effect of the peroxisome proliferator-activated receptor (PPAR)-{gamma} agonist rosigliotazone on the induction of endometriosis in a rat model.

Methods: Endometriosis was surgically induced in 28 rats by transplanting an autologous fragment of endometrial tissue onto the inner surface of the abdominal wall. Group I was assigned as control and no medication was administered. Starting 3 days before the operation and continuing for 4 weeks, 0.2 mg/kg/d rosiglitazone was administered to the study group orally. Four weeks later rats were killed and ectopic uterine tissues were evaluated morphologically and histologically. Scoring systems were used to evaluate preservation of epithelia.

Results: Four rats in the study group and one rat in the control group died of complications related to surgery. There was a significant difference in post-treatment spherical volumes (64.00 mm3 [interquartile range (IQR): 354.42] vs 41.60 mm3 [IQR: 37.87], P = .018) and explant weights (77.97 mg [IQR: 431.27] vs 47.24 mg [IQR: 43.01], P = .005) between control and rosiglitazone-treated groups. The epithelia were found to be preserved significantly better in the control group when compared with the roziglitazone-treated group (2.00 [IQR:2.00] vs 0.00 [IQR:2.25], P = .014).

Conclusions: Rosiglitazone was found to affect the induction of endometriosis negatively in this experimental rat model and seemed to interfere with the growth and maintenance of the uterine explant.

Key Words: Rosiglitazone • experimental endometriosis model • rat • peroxisome proliferator-activated receptor


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