Background Polycystic ovary syndrome (PCOS) is a multifactorial endocrine disease, which is an important cause of female infertility worldwide. PCOS patients are in a state of chronic low-grade inflammation, and immune imbalance is considered as a potential cause of its pathogenesis. Methods The expression of AOC4P in PCOS and normal ovarian granulosa cells (GCs) was detected by real-time quantitative PCR. KGN cells were induced by dihydrotestosterone at 500 ng/ml to construct PCOS model. After lentivirus-infected, KGN cells were constructed with AOC4P overexpression cell lines, the proliferation and apoptosis levels of KGN cells in AOC4P and NC groups were detected. THP-1-derived macrophages and peripheral blood mononuclear cells (PBMC) were co-cultured with KGN cells for 48h respectively, and the differentiation of macrophages and CD4 + T cells were detected by flow cytometry. Results Decreased AOC4P expression was found in PCOS patients. After constructing PCOS cell model, we observed that overexpression of AOC4P promoted KGN cell proliferation and inhibited apoptosis. After co-culture with AOC4P overexpressed KGN cells, M1 macrophages decreased, M2 macrophages increased, Th1/Th2 ratio increased, and Treg cells increased. Finally, we found that AOC4P inhibited the activation of the nuclear factor κ B (NFκB) pathway in KGN cells. Conclusions In this study, we found that AOC4P regulated the NFκB signaling pathway by inhibiting the phosphorylation of P65, thereby affecting the proliferation and apoptosis of GCs, altering the differentiation of macrophages and T cells, and contributing to the pathogenesis of PCOS.

Background Polycystic ovary syndrome (PCOS) is a multifactorial endocrine disease, which is an important cause of female infertility worldwide. PCOS patients are in a state of chronic low-grade inflammation, and immune imbalance is considered as a potential cause of its pathogenesis. Methods The expression of AOC4P in PCOS and normal ovarian granulosa cells (GCs) was detected by real-time quantitative PCR. KGN cells were induced by dihydrotestosterone at 500 ng/ml to construct PCOS model. After lentivirus-infected, KGN cells were constructed with AOC4P overexpression cell lines, the proliferation and apoptosis levels of KGN cells in AOC4P and NC groups were detected. THP-1-derived macrophages and peripheral blood mononuclear cells (PBMC) were co-cultured with KGN cells for 48h respectively, and the differentiation of macrophages and CD4 + T cells were detected by flow cytometry. Results Decreased AOC4P expression was found in PCOS patients. After constructing PCOS cell model, we observed that overexpression of AOC4P promoted KGN cell proliferation and inhibited apoptosis. After co-culture with AOC4P overexpressed KGN cells, M1 macrophages decreased, M2 macrophages increased, Th1/Th2 ratio increased, and Treg cells increased. Finally, we found that AOC4P inhibited the activation of the nuclear factor κ B (NFκB) pathway in KGN cells. Conclusions In this study, we found that AOC4P regulated the NFκB signaling pathway by inhibiting the phosphorylation of P65, thereby affecting the proliferation and apoptosis of GCs, altering the differentiation of macrophages and T cells, and contributing to the pathogenesis of PCOS.