【摘要】 多囊卵巢综合征（polycystic ovary syndrome,PCOS）是以高雄激素表型为典型特征的育龄期女性常见的内分泌疾病，其发病机制尚不明确，现多认为雄激素对其发病具有重要影响。双酚A(bisphenol A,BPA)作为环境内分泌干扰物，能够上调相关雄激素合成酶的表达，通过过量雄激素暴露来诱导PCOS的发生。研究表明BPA暴露能够抑制芳香化酶的活性，阻止雄激素与受体的结合，从而诱导高雄激素血症。BPA还可通过氧化应激、雌激素相关途径、下丘脑-垂体-卵巢轴以及对肥胖和胰岛素抵抗的调节等途径调控PCOS患者的卵巢功能。综述BPA通过调控高雄激素诱发PCOS的神经内分泌机制及相关信号通路，以期阐述BPA具体的生物学功能，为后续研究提供参考。更多还原

【Abstract】 Polycystic ovary syndrome(PCOS) is a common endocrine disease characterized by hyperandrogenic phenotype in women of reproductive age. The pathogenesis of PCOS remains unclear, and androgen is now thought to have an essential impact on the pathogenesis of PCOS. Bisphenol A(BPA), an environmental endocrine disruptor, can increase the relevant androgen synthetase and induce PCOS through excessive androgen exposure. Studies have shown that BPA exposure can inhibit the activity of aromatase, prevent the binding of androgen and receptor, thus inducing hyperandrogenemia. BPA can also regulate the ovarian function of PCOS through oxidative stress, estrogen-related pathways, hypothalamic-pituitary-ovarian axis, regulation of obesity and insulin resistance, and other routes. This article aims to review the neuroendocrine mechanism and related signal pathways of BPA-induced PCOS by regulating hyperandrogen, clarify the specific biological functions of BPA and provide a reference for follow-up research.更多还原