Edible bird's nest ameliorates hyperandrogenism and gonadotropin imbalance in a rat model of polycystic ovary syndrome

食用燕窝可改善多囊卵巢综合征大鼠模型中的高雄激素血症和促性腺激素失衡。

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Abstract

Edible bird's nest (EBN) is a traditional functional food consumed for its purported reproductive health benefits. However, robust preclinical evidence supporting its efficacy in polycystic ovary syndrome (PCOS)-a prevalent endocrine disorder characterized by hyperandrogenism and gonadotropin dysregulation-is lacking. This study aimed to evaluate the effects of a commercially available fresh EBN product on reproductive endocrine, metabolic, and ovarian parameters in a letrozole-induced PCOS rat model. Female Sprague-Dawley rats were divided into 6 groups (n = 8/group): blank control, PCOS model control, normal control, low-dose EBN (5 mg/kg/day), medium-dose EBN (10 mg/kg/day) high-dose EBN (20 mg/kg/day). PCOS was induced by subcutaneous letrozole (1 mg/kg/day) combined with a high-fat/high-sucrose diet for 21 days, followed by 28 days of oral intervention. Estrous cyclicity, serum sex hormones (LH, FSH, testosterone, estradiol), glucose tolerance (OGTT), systemic inflammation, and ovarian histopathology were assessed. EBN treatment significantly ameliorated hyperandrogenism and gonadotropin imbalance in PCOS rats: it reduced elevated serum luteinizing hormone (LH) and testosterone levels, lowered the LH/FSH ratio, and increased suppressed follicle-stimulating hormone (FSH) and estradiol (all p < 0.05 vs. model control). However, these endocrine improvements were not accompanied by restoration of regular estrous cyclicity, reversal of polycystic ovarian morphology, or improvement in glucose intolerance. No significant changes in systemic inflammatory markers were observed. Oral administration of fresh edible bird's nest effectively corrects key reproductive hormonal disturbances in a rat model of PCOS. While these findings support a potential role for EBN as a dietary modulator of the hypothalamic-pituitary-ovarian axis, its inability to restore ovulatory function or metabolic parameters underscores the complexity of PCOS pathophysiology and the need for multifaceted therapeutic approaches.

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