| Objective: Postnatal treatment of female rats with andro^n results in subsequent infertility. The mechanism of hyperandrogenism and chronic anovulation in androgen-sterilized rats(ASR) is unclear. 1.The present study was designed to establish ASR animal model, to determine body weight, fasting glucose and insulin , serum testosterone levels, to compare the pathological changes of ovary and adrenal , to evaluate the distinction between ASR and polycystic ovary syndrom (PCOS). 2. To determine inhibin a subunit and follistatin gene expression in ovary^ pituitary N hypothalamus and adrenal, to explore whether they play roles in the etiology of ASR.Methods: Thirty 9 days'old SD female rats were divided randomly into2 groups. The rats of one group were given a single subcutaneous injection of 1.25 mg of testosterone propionate. The rats of the other group were injected the same quantity tea oils. At 100 days of age, body weight .fasting glucose and insulin ,serum testosterone levels were determined. Ovarian and adrenal morphology were observed with naked eyes and optical microscope. Semi-quantitative RT-PCR was used to detect the mRNA expression of follistatin and inhibin a subunit in ovary, pituitary ^hypothalamus and adrenal.Results:1. Body weight, fasting glucose and insulin , serum testosterone levels were significantly higher in the ASR than those in the control. ( body weight:208± 17. 4 vs 136±26. l(g),-ASR vs control; fasting glucose:11. 79 ± 0.61 vs 4.82 ± 0.31(mlU/L), ASR vs control; fasting insulin:59.3 ±7.1 vs 17 ± 3.6(mIU/L), ASR vs control; serum testosterone:4. 50 ± 1.75 vs 1. 77 ± 0. 60( u g/L), ASR vs control) (p<0.01)2.The ASR ovary had a number of cystic follicles, reduced granulosa cell layers. Corpora lutea and oocyte were absent. The width ofreticular zona were enhanced and blood vessels' hyperplsia wereevident.3. Follisatin gene expression in ovary and adrenal of ASR was higher than that of control. ( ovary:1. 22±0.15 vs 0. 74±0. 07, ASR vs control; adrenal: 1. 43 ± 0. 03 vs 0. 68 ± 0. 04, ASR vs-control) ( p<0. 05, p<0. 01, respectively) Inhibin a subunit gene expression in ova^ pituitary and adrenal of ASR was higher than that of control. ( ovary:3. 73±0. 93vs 1. 59 ± 0.12, ASR vs control; pituitary : 1. 52 ± 0. 26 vs 0. 99 ± 0. 31, ASR vs control; adrenal: 1.46 ± 0.17 vs 0.73±0.10, ASR vs control) ( p<0. 01, p<0. 05, p<0. 05, respectively)There was no notable difference of follisatin gene expression in pituitary between the ASR and control . (0.29 ± 0. 04vsO. 30 ± 0.06, ASR vs control , p=0.605)There were no notable differences of follisatin and inhibin a subunit gene expression in hypothalamus between the ASR and control, (follistatin: 0. 34±0. 05 vs 0. 35 ±0.05, ASR vs control; inhibin a subunit:0. 34±0.05 vs 0. 35±0. 06, ASR vs control)( p=0.497, p=0.481, respectively)4. Regression analysis demonstrated that serum testosterone levels were positively correlated with follistatin and inhibin a subunit mRNA expression in ovary and adrenal. (r,=0. 887, r2=0. 625, r3=0. 694, r<=0. 525, p<0. 05)Conclusion:1. The current reseach suggested ASR had the hyperandrogenism and anovulation features of PCOS, so ASR can berecognized as a hyper androgenic hyperinsulinic anovulation animal model. 2. Follistatin and inhibin a subunit gene expression in ovary^ pituitary and adrenal show that they might play roles in the mechanism of hyperandrogenism and anovulation of ASR by autocrine > paracrine and endocrine manner. |
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