Polycystic ovary syndrome (PCOS) is a common chronic inflammatory metabolic disease in women of reproductive age, and is considered as a potential risk factor for infertility because it is often characterized by insufficient or non-ovulation, and over 70% of patients suffer from hyperandrogenemia. High androgen levels not only inhibit follicular growth, promote premature luteinization of follicles, hinder the selection of dominant follicles, but also induce the formation of inflammation, which is an important factor for PCOS to maintain chronic inflammatory state. Abnormally high LH pulses reflect the overactivity of GnRH neural circuit, reflecting the neuroendocrine basis of the etiology or phenotype of PCOS. Kisspeptin secreted by brain neurons not only promotes androgen-related chronic inflammation by activating GnRH, but also directly inhibits the production of NK cells, such as IL-4, IL-10, and IFN. Melatonin reduces androgen levels, inhibits inflammatory factors and improves oocyte quality through the extracellular signal-regulated kinase pathway of granulosa cells. C1QTNF6, a newly identified inflammatory adiponectin byproduct, affects inflammatory responses through the AKT/NF-κB signaling pathway and may be a good new diagnostic target of PCOS. This paper reviewed the relationship between neuro-endocrine regulation and inflammatory factors, and found that the upstream nerve of hypothalamus can promote the formation of hyperandrogenemia by regulating the hypothalamic-pituitary-gonad axis, which leads to the occurrence of inflammation and participate in the occurrence and development of PCOS. Meanwhile, melatonin, GNRH-AAB and C1QTNF6 may be new targets for the treatment or diagnosis of PCOS. It is hoped that this can provide some new ideas for the research of PCOS.