Abstract

Mice of FRBI-1, FRBI-2, and FRBI-3 groups were intramuscularly injected with 20, 30, and 40mg/kg, respectively, for five consecutive days. Ovarian weights of three FRBI groups were reduced in comparison with FSH group. Ovarian cortex thicknesses (OCT) of the FRBI-3 group were less than that of the FSH group (P<0.05). As compared to FSH group, there were fewer numbers of secondary follicles (SFs) and mature follicles (MF) on the ovaries of FRBI-treated mice numbers of primary follicles (PFs) and SFs also decreased. In FRBI-3 mice, we found that the primordial follicles (POF) were scarcer, the follicles developed poorly, and granulosa cells became apoptosis. SF numbers of FRBI-2 and FRBI-3 groups were less than that of the FSH group on day 20 (P<0.05). Maximum longitudinal diameter (MLD) and transverse diameter (MTD) of three FRBI groups became decreased during the experiment. MLD and MTD of the FRBI-3 group were smaller than FSH group. Levels of FSHR mRNA and protein were less than that of CG and FSH group (P<0.05). ERα protein levels of FRBI group and serum concentrations of FSH and estradiol (E2) in the FRBI-treated mice were decreased when compared to CG and FSH group. In conclusion, FSH treatment could increase the numbers of SF and MF, enhance follicle development, reduce the numbers of SF and MF, and depress the follicular development of mice. Furthermore, FRBI declined the mRNA and protein levels of ERα and FSHR in the ovaries and dropped serum concentrations of FSH and E2 of mice.

Highlights

  • Follicle stimulating hormone (FSH) and estradiol (E2) can precisely regulate the female fertility depending on the development of ovarian follicles and final ovulation [1, 2]

  • FSH receptor binding inhibitor (FRBI) of 20, 30, and 40mg/kg body weight were intramuscularly injected into the mice of FRBI-1, FRBI-2, and FRBI-3, respectively, for five consecutive days. 10IU FSH was intramuscularly injected into mice of FSH group for five consecutive days. 0.2mL saline was injected into mice of control group (CG) for five consecutive days

  • These results demonstrated that FSH treatment could increase the numbers of secondary follicles (SF) and mature follicles (MF), enhancing follicle development

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Summary

Introduction

Follicle stimulating hormone (FSH) and estradiol (E2) can precisely regulate the female fertility depending on the development of ovarian follicles and final ovulation [1, 2]. FSH receptor binding inhibitor (FRBI) blocked the combination of FSH into FSHR and inhibited FSH action on at the gene and protein levels [5, 6]. The roles of ERα and ERβ in reproductive function remain undecided [13]. Up to date, it remains unclear if FRBI treatment impacts the expression levels of estrogen receptors in the ovarian follicles [14, 15]. The present work was performed to assess the effects of FSH receptor binding inhibitor (FRBI) on the development of ovaries and follicles and reproduction functions, to understand the FRBI mechanism of inhibiting the interaction of FSH to FSHR in the follicles, and to investigate the signal transduction and pathway of FRBI actions in mice

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