menotropins and Disease-Models--Animal

Medroxyprogesterone 17-acetate (MPA) combined with human menopausal gonadotropin (hMG) has been effectively used for ovarian stimulation in clinical practice. However, the molecular mechanism of MPA + hMG treatment in follicular development is poorly described. Here we performed a study to investigate the impact of MPA + hMG on ovarian stimulation utilizing a mouse model in vivo. Forty female BALB/C mice were randomly divided into four groups of 10 each and treated during ciestrus stage and continued for 5 days: control group, MPA group, hMG group, and MPA + hMG group. Morphological and molecular biology methods were used for detecting serum hormones and ovarian function. MPA + hMG group exhibited increasing follicle stimulating hormone (FSH), antral follicle, FSH receptor (FSHR) and phosphorylated mammal target of rapamycin (p-mTOR), and decreasing luteinizing hormone (LH), estradiol (E2), progesterone (P), corpus luteum, phosphoinositide 3-kinase (PI3K), Akt and mTOR compared with control group. In contrast, MPA + hMG group showed reduced FSH, LH, E2, P, corpus luteum, LH receptor (LHR), and activated PI3K,/Akt/mTOR pathway compared with hMG group (P < 0.05). Collectively, these data definitively established that MPA plus hMG may modulate the hormone, hormone receptor and PI3K/Akt/mTOR signaling pathway to influence follicular development in the mouse ovary. Our study provides overwhelming support for MPA + hMG as an effective treatment for infertility in women.

Topics: Animals; Disease Models, Animal; Female; Hormones; Humans; Medroxyprogesterone Acetate; Menopause; Menotropins; Mice; Mice, Inbred BALB C; Ovarian Follicle; Ovulation Induction; Random Allocation; Signal Transduction; Treatment Outcome

Hormonal indices, phase pattern of estrous cycles, and histological structure of the ovaries were studied in female rats with polycystic ovaries caused by subcutaneous implantation of Silastic capsules with testosterone after consecutive treatment with non-steroid antiandrogen, flutamide (flutafarm), urinary FSH (menopur) and HCG (choragon). It was shown that while the plasma testosterone level was increased, administration of the drugs in subtherapeutical doses interrupted persistent diestrus, renewed estrous cycle, gonadal and uterine weights, induced appearance of postovulatory luteal bodies and restored fertility. Therefore, antiandrogen potentiation of pharmnnaco-dynamic effect of the gonadotropins with regard to their ability to ovulation induction was found out.

Topics: Androgen Antagonists; Androgen Receptor Antagonists; Animals; Anovulation; Chorionic Gonadotropin; Disease Models, Animal; Estrus; Female; Fertility Agents, Female; Flutamide; Menotropins; Ovulation; Polycystic Ovary Syndrome; Rats; Rats, Wistar; Receptors, Gonadotropin; Testosterone

Human menopausal gonadotropin (hMG, 75 IU/body/day) and a gonadotropin-releasing hormone (GnRH) agonist buserelin (1, 10, 100 microg/kg/day) were simultaneously administered to female rabbits by the subcutaneous route for 7 days, and the effects on organ weights, plasma hormones and weight of ascitic fluid were examined. Treatment with hMG increased the ovarian weight, plasma estradiol and weight of ascites, thus indicating that ovarian hyperstimulation syndrome had been induced. Simultaneous treatment with buserelin decreased the changes induced by hMG. GnRH agonists can thus be surmised to reduce the severity of ovarian hyperstimulation syndrome in the rabbit. However, caution is needed when extrapolating the results of this rabbit model to humans.

Topics: Animals; Ascites; Buserelin; Disease Models, Animal; Dose-Response Relationship, Drug; Drug Therapy, Combination; Estradiol; Female; Gonadotropin-Releasing Hormone; Menotropins; Organ Size; Ovarian Hyperstimulation Syndrome; Ovary; Progesterone; Rabbits; Uterus

Ovarian hyperstimulation was produced by human menopausal gonadotropin and chorionic gonadotropin in rabbits. A more rapid regression of the hyperstimualted ovaries was observed in an antihistamine-treated group than in a control group. The difference in regression was found to be statistically significant. The possibility of treating the ovarian hyperstimulation syndrome by antihistamine is cited.

Topics: Animals; Chorionic Gonadotropin; Disease Models, Animal; Female; Histamine H1 Antagonists; Iatrogenic Disease; Menotropins; Ovarian Diseases; Rabbits; Syndrome

Topics: Animals; Ascitic Fluid; Chlorpheniramine; Disease Models, Animal; Female; Humans; Menotropins; Ovarian Cysts; Ovarian Diseases; Ovary; Pleural Effusion; Rabbits