Abstract
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.
Highlights
Infertility is one of the most common diseases in the world
In the Medroxyprogesterone 17-acetate (MPA) + human menopausal gonadotropin (hMG) group, there is a significantly increase in follicle stimulating hormone (FSH) level and decreases in luteinizing hormone (LH), E2 and P levels compared to the control group (P < 0.05), FSH level is higher in MPA + hMG group than the MPA group
We generated a BALB/C mouse model of clinical MPA + hMG treatment to delineate whether this treatment have positive effects on follicular development, through regulation of ovarian hormones, their receptors and the involvement of the phosphoinositide 3-kinase (PI3K)/Akt/mTOR pathway on follicular development during ovarian hyperstimulation
Summary
Infertility is one of the most common diseases in the world. Currently, more and more patients have to seek help from assisted reproductive therapy (ART) to have their own child[1]. The administration of gonadotropin-releasing hormone (GnRH) analogues, including GnRH agonists and GnRH antagonists, is used for preventing premature LH surges in pituitary desensitization among infertile patients in conventional controlled ovarian hyperstimulation[2]. This therapy has proven to have some limits because of the increased incidence of ovarian hyperstimulation syndrome (OHSS) by GnRH agonists and the rate of premature LH surges (0.34–38.3%) via GnRH antagonists[3,4]. The the administration of P during follicular phase had no negative effect on oocyte retrieval rates of the hMG + MPA treatment cycles based on frozen embryo transfer[12]. Based on our own and others’ work, we developed a mouse model of MPA + hMG treatment to investigate the role of MPA + hMG in follicular development and hypothesized that MPA + hMG may promote follicular development by regulating ovarian hormones, hormone receptors and PI3K/Akt/mTOR signaling pathways
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