P-214: Testosterone to Induce Mice Models for The Study of Polycystic Ovary Syndrome

Background: Polycystic ovary syndrome (PCOS) is one of the most common causes of anovulation, infertility and hyperandrogenism in women, affecting 5-10% of women of reproductive age. Due to the ethical limitations on human experimentation, appropriate animal models that mimic many or all PCOS characteristics would facilitate research leading to improved understanding of the pathogenesis of PCOS and potential for curative treatments for the PCOS syndrome. During the last years some various animal models used for the study of PCOS have allowed a focus on different aspects of the pathology. Numerous experimental models for PCOS have been developed in rodent. Rodents are clearly precious models to assess disruption of fertility. Rodent models are inexpensive, and provide well-characterised and stable genetic backgrounds readily accessible for targeted genetic manipulation, as well as shorter reproductive lifespan and generation time. Recent rodent models display both reproductive and metabolic disturbances associated with human PCOS. To date, various methods used to induce PCOS models. So, we made a PCO mouse model with testosterone injection and assessed ovarian morphological and hormonal aspects polycystic ovary. Materials and Methods: In this study, fifteen female prepuberal (20 day-old) mice of the C57 strain were daily injected (sc) with 1mg/kg body weight testosterone for 30 consecutive days. FSH, LH and testosterone serum levels measured by ELISA kit. Ovaries were dissected and fixed in 10% buffered formalin during 24 hours at room temperature. After fixation and alcohol dehydration the paraffin sections were first examined following the hematoxylineosin (HandE) staining. Results: Our results showed serum testosterone levels in PCO model group were significantly higher than that of control group (1.57 ± 0.7 vs. 0.25 ± 0.1 ng/ml). LH and FSH levels in two groups were not different. We assessed 4 sections of each ovaries and counted follicle number. Ovarian morphological features showed that early antral and antral follicle count in PCO model was 2.31 ± 0.36 and 3.62 ± 0.29, it was significantly higher than that of control group (1 ± 0.2 and 0.78 ± 0.6 respectively). Granulosa and techa layers thicknesses were measured and compared. Our results demonstrated granulosa/techa ratio was significantly higher in control than that of PCO model (4.06 ± 0.4 vs. 2.67 ± 0.1 respectively). In control group ovaries was observed corpus luteum (CL) but in PCO model we did not detect any CL. Conclusion: We could make a PCO model that ovarian morphology would be similar to polycystic ovary without ovulation. In addition, the increase of androgen level similar to polycystic ovarian syndrome was observed. Nevertheless, decreasing of LH level in our PCO model was different from polycystic ovarian syndrome characteristics. Granulosa thickness reduction in our model determined decreasing of estrogen production made of androgenic environment of follicles. So, with this method, a PCO mouse model can be made. It has some polycystic ovarian syndrome characteristics.