Polycystic ovary syndrome (PCOS) is a clinical syndrome characterized by hyperandrogenism, oligo/anovulation, and polycystic ovary. Autophagy is an intracellular system that degrades cytosolic proteins and organelles. The relationship between autophagy and PCOS has not been clarified. We found that p62 and ubiquitin were significantly increased in theca cells of women with PCOS using immunohistochemistry. Autophagy inhibition by palmitic acid and chloroquine in bovine theca cells increased p62 and ubiquitin and induced the expression of cytochrome P450 17A1 (CYP17A1) and plasminogen activator inhibitor-1 (PAI-1) mRNA. Furthermore, palmitic acid and chloroquine exposure significantly increased reactive oxygen species (ROS) and activated p38 and c-Jun N-terminal kinase (JNK). Inhibition of p38 and JNK significantly reduced CYP17A1 and PAI-1 mRNA expression. We showed that inhibition of autophagy in theca cells may have contributed to the pathogenesis of PCOS, based on CYP17A1 and PAI-1 mRNA expression via the ROS/p38 and JNK signalling pathways.

中文翻译：

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在多囊卵巢综合征的发展过程中，抑制吞噬细胞中的自噬可通过ROS / p38和JNK信号传导诱导CYP17A1和PAI-1的表达。

多囊卵巢综合征（PCOS）是一种以高雄激素症，寡排卵/无排卵和多囊卵巢为特征的临床综合征。自噬是一种细胞内系统，可降解胞质蛋白和细胞器。自噬与PCOS之间的关系尚未阐明。我们发现，使用免疫组织化学技术，PCOS妇女的卵泡膜细胞中p62和泛素显着增加。牛卵泡膜细胞中棕榈酸和氯喹的自噬抑制作用增加了p62和泛素，并诱导了细胞色素P450 17A1（CYP17A1）和纤溶酶原激活物抑制剂1（PAI-1）mRNA的表达。此外，棕榈酸和氯喹的暴露显着增加了活性氧（ROS）并激活了p38和c-Jun N端激酶（JNK）。抑制p38和JNK会显着降低CYP17A1和PAI-1 mRNA的表达。我们显示，基于经由ROS / p38和JNK信号通路的CYP17A1和PAI-1 mRNA表达，抑制卵泡膜细胞自噬可能与PCOS的发病机理有关。