Objective: In humans, polycystic ovary syndrome (PCOS) is an androgen-dependent ovarian disorder. Aberrant gene expression in folliculogenesis can arrest the transition of preantral to antral follicles, leading to PCOS. We explored the possible role of altered gene expression in preantral follicles of estradiol valerate (EV) induced polycystic ovaries (PCO) in a mouse model.Methods: Twenty female balb/c mice (8 weeks, 20.0±1.5 g) were grouped into control and PCO groups. PCO was induced by intramuscular EV injection. After 8 weeks, the animals were killed by cervical dislocation. Blood serum (for hormonal assessments using the enzyme-linked immunosorbent assay technique) was aspirated, and ovaries (the right ovary for histological examinations and the left for quantitative real-time polymerase) were dissected. Results: Compared to the control group, the PCO group showed significantly lower values for the mean body weight, number of preantral and antral follicles, serum levels of estradiol, luteinizing hormone, testosterone, and follicle-stimulating hormone, and gene expression of TGFB1, GDF-9 and BMPR2 (p<0.05). Serum progesterone levels were significantly higher in the PCO animals than in the control group (p0.05) were found in BMP6 or BMP15 expression. Conclusions: In animals with EV-induced PCO, the preantral follicles did not develop into antral follicles. In this mouse model, the gene expression of TGFB1, GDF9, and BMPR2 was lower in preantral follicles, which is probably related to the pathologic conditions of PCO. Hypoandrogenism was also detected in this EV-induced murine PCO model.

Background: Endometriosis can lead to infertility. Since there is no definitive treatment for endometriosis, animal modelling seems necessary to examine the possible treatments. Mouse endometrium cannot be separated for endometriosis induction. In addition, transplantation of uterus into the abdominal viscera to induce endometriosis causes organ damage. In this study, we defined a new model of endometriosis leading to separability of endometrium and a safe anatomical region for transplantation.Methods: Forty female mice were allocated to 5 groups: 1, sham; 2, allograft uterus transplantation of mice to anterior abdominal wall of mice; 3, allograft uterus transplantation of mice to mesentery of mice; 4, xenograft endometrial transplantation of rat to anterior abdominal wall of mice; 5, xenograft endometrial transplantation of rat to mesentery of mice. Adult female rats with a previous pregnancy experience were selected and placed in the vicinity of male rats for 2 weeks to induce estrogen secretion and increase endometrial thickness.Results: In the 4th group of animals, compared to sham, the peritoneal concentrations of VEGF‐A, TNF‐α, NO, MDA, and serum levels of CA‐125 and IL‐37 were increased and total body weight was decreased, while weight and size of endometrial lesions were increased significantly (P < .05). Genes expression of HOXA10 and HOXA11 were decreased significantly (P < .05) in groups 2 and 4 compared to sham.Conclusions: Xenograft transplantation of endometrium from rat to anterior abdominal wall of mice can potentially mimic human endometriosis morphologically, histologically, and genetically.

Cisplatin is a chemotherapeutic medication that also exhibits toxic effects on normal cells. Acacetin (ACA) is an herbal compound that exhibits anticancer properties with few side effects. We investigated the use and side effects of ACA and cisplatin on the male reproductive system. Mature male mice were divided into six groups: control group treated with DMSO, cisplatin group treated with 1 mg/kg cisplatin and three ACA groups treated with 10, 25 or 50 mg/kg ACA. All treatments were applied for three days. A final experimental group was treated with 50 mg/kg ACA for 10 days. At the end of the experiment, animals were sacrificed and reactive oxygen species (ROS), total antioxidant capacity (TAC), OCTN3 gene expression and apoptosis were measured in testis. TAC and OCTN3 gene expression were decreased, while ROS and apoptosis were increased in cisplatin group compared to other groups. All ACA groups exhibited decreased apoptosis and ROS levels, and increased TAC and OCTN3 gene expression compared to the cisplatin treated mice. ACA caused fewer adverse effects in testicular tissue than cisplatin. ACA appears to improve the oxidant-antioxidant system, accelerates cell regeneration and inhibits apoptosis.