Abstract
The exact pathogenesis of polycystic ovary syndrome (PCOS), the most common neuroendocrine disorder in women of reproductive age, has not been fully elucidated. Recent studies suggested that chronic inflammation and neurotransmitter disorder involved in the progress of PCOS. Troxerutin, a natural flavonoid, was reported to possess neuroprotective effect in several disease models by inhibiting inflammation or enhancing neurotrophic factor. In this study, we investigated the possible protective effect and mechanism of troxerutin in a dihydrotestosterone (DHT)-induced rat model of PCOS. The PCOS rat models were treated with troxerutin at a dose of 150 mg/kg or 300 mg/kg for up to 4 weeks. Results showed that 300 mg/kg troxerutin significantly decreased the body weight gain and improved the pathological changes of ovary induced by DHT. Meanwhile, the elevated gonadotrophin-releasing hormone (GnRH), gonadotrophin and testosterone in the serum of PCOS rats were reduced with the treatment of troxerutin. The expression of kisspeptin and NKB in arcuate nucleus and their receptors kiss1r and NK3r in GnRH positive neurons of median eminence were markedly decreased in troxerutin-treated rats. Of note, the GnRH inhibitory regulator GABA and stimulatory regulator glutamate were also restored to the normal level by troxerutin. The present study indicated that troxerutin may exhibit a protective effect in PCOS rat model via regulating neurotransmitter release.
Highlights
Polycystic ovary syndrome (PCOS) is a reproductive endocrinopathy with the prevalence estimated to be 6% ~ 20%(depending on the different diagnostic criteria used), making it the most common endocrine condition in women of reproductive age [1]
Since ovarian histological change is another feature of PCOS, we investigated whether troxerutin improved histological structure in rat ovaries
We furthered calculated the percentage of follicles of total and the results showed that PCOS rats exhibited significantly increased primordial and decreased primary follicles as compared to sham rats(P < 0.001; P < 0.001), and troxerutin 300 mg/kg inhibited the markedly low percentage of primary follicles in PCOS rats(P < 0.05)
Summary
Polycystic ovary syndrome (PCOS) is a reproductive endocrinopathy with the prevalence estimated to be 6% ~ 20%(depending on the different diagnostic criteria used), making it the most common endocrine condition in women of reproductive age [1]. The diagnostic features of PCOS include androgen excess, ovulatory dysfunction and polycystic ovaries [1]. 30–60% of PCOS patients, depending on the country of origin [2, 3]. The most consistent biochemical abnormality in women with PCOS is hyper-secretion of androgen, elevated serum luteinizing hormone (LH) levels and low to normal serum follicle stimulating hormone (FSH) levels [4, 5]. Animal models that reflect PCOS features are crucial resources to investigate this syndrome. A chronically 5α-dihydrotestosterone (DHT)-treated rat model closely mimics the human PCOS phenotype and is a suitable model for investigations about PCOS
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