Abstract
This study aimed to investigate whether chronic unpredictable mild stress (CUMS) affects follicular development in ovaries through the nerve growth factor (NGF)/high affinity nerve growth factor receptor, the Tropomyosin-related kinase A (TrkA) receptor, mediated signaling pathway and to reveal the relationship between chronic stress and premature ovarian insufficiency (POI) development. In this experiment, a CUMS rat model was constructed. It was found that serum estradiol (E2), anti-Mullerian hormone (AMH), and gonadotropin-releasing hormone (GnRH) levels decreased, while follicle-stimulating hormone (FSH) levels increased. The expression of NGF, TrkA, p75, and FSHR in ovarian tissue decreased significantly. The expression levels of TrkA and p75 protein in ovarian stroma and small follicles were observed by an immunofluorescence assay. In addition, the numbers of small follicles were significantly reduced. The expression of TrkA, p75, and FSHR in CUMS ovarian tissue was upregulated by exogenous NGF in vitro. Furthermore, after treatment with NGF combined with FSH, E2 secretion in ovarian tissue culture supernatant of CUMS rats also increased significantly. Therefore, CUMS downregulates NGF and TrkA and promotes the occurrence of POI in rats. Exogenous NGF and FSH can upregulate the NGF receptor, E2, and AMH in vitro, and improve the rat ovarian function. Future studies may associate these results with female population.
Highlights
In recent years, premature ovarian insufficiency (POI) has become an increasingly prominent problem in the field of female reproductive health
There was no significant difference between the two groups in the E2, antiMullerian hormone (AMH), gonadotropin-releasing hormone (GnRH), and follicle-stimulating hormone (FSH) levels
The levels of E2, AMH, and GnRH on day 35 were significantly lower (P < 0:05), while the levels of FSH were significantly higher in the chronic unpredictable mild stress (CUMS) group than in the control group (P < 0:01; Figure 1)
Summary
Premature ovarian insufficiency (POI) has become an increasingly prominent problem in the field of female reproductive health. There are few studies on the effect of psychological stress on ovarian function. Some animal studies have found that chronic unpredictable mild stress (CUMS) can lead to the decrease of ovarian reserve in C57BL/6 mice [5] and SD rats [6]. These studies show that stress does have an effect on ovarian function. The mechanism of how psychological stress leads to the decrease of ovarian reserve, even to ovarian dysfunction
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