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Updated: Jul 14, 2026
Mouse Model of Surgically-induced Endometriosis by Auto-transplantation of Uterine Tissue
Published on: January 6, 2012
Genistein causes regression of endometriotic implants in the rat model
Emrah Yavuz1, Mesut Oktem, Ibrahim Esinler
1Department of Obstetrics and Gynecology, Baskent University Faculty of Medicine, Ankara, Turkey.
Objective:
To determine the effects of raloxifene and genistein on experimentally induced endometriosis in a rat model.
Design:
Prospective, randomized animal study.
Setting:
Animal surgery laboratory in a university hospital.
Animal(S):
Thirty-three adult, mature female Wistar-Albino rats in which endometriotic implants were induced by transplanting autologous uterine tissue to ectopic sites on the peritoneum.
Intervention(S):
After the endometriotic implants were formed surgically, the 33 rats were randomly divided into three groups. Group 1 (genistein group, 10 rats) were given 500 mg/kg per day of oral genistein. Group 2 (raloxifene group, 10 rats) were given 10 mg/kg per day of oral raloxifene. Group 3 were given no medication and served as controls (13 rats). All the rats continued to receive treatment for 21 days, and then were killed to assess the implants' size and for histologic examination.
Main Outcome Measure(S):
The surface area of the endometriotic implants and the score of histologic analysis.
Result(S):
At the beginning of the medical treatment, the mean surface areas of the endometriotic implants were comparable in all three groups. At the end of the medical treatment, the mean surface area of implants in groups 1 and 2 was smaller than that of implants in the control group. The decrease in the surface area of the endometriotic implants was greater in group 1 and group 2 than found in the control group. The histologic assessment revealed that the mean of the histopathologic score of the implants at the end of the treatment was lower in groups 1 and 2 when compared with the control group.
Conclusion(S):
Genistein caused a statistically significant regression of endometriotic implants.
