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Abstract：
Polycystic ovary syndrome (PCOS) is a globally prevalent gynecological disorder among women of childbearing age. The present study aimed to investigate the role of tenascin C (TNC) in PCOS and its potential mechanisms. Fasting blood glucose and serum insulin, the homeostasis model assessment of insulin resistance and the serum hormone levels were determined in PCOS rats. In addition, H&E staining was used for assessing pathology. In addition, the effects of TNC on oxidative stress and inflammation response in PCOS rat and cell models was assessed. Furthermore, the roles of TNC on KGN cell proliferation and apoptosis were determined employing EdU assay and flow cytometry. TLR4/NF‑κB pathway‑related proteins were measured using western blotting, immunofluorescence and immunohistochemistry. It was found that the mRNA and protein expression was upregulated in PCOS rats and in KGN cells induced by dihydrotestosterone (DHT). Knockdown of TNC relieved the pathological characteristics and the endocrine abnormalities of PCOS rats. Knockdown of TNC inhibited ovarian cell apoptosis, oxidative stress and inflammation in PCOS rats. Knockdown of TNC reversed the DHT‑induced reduction in cell proliferation and increase in apoptosis in KGN cells. Furthermore, knockdown of TNC alleviated oxidative stress and inflammatory responses induced by DHT in KGN cells. Additionally, knockdown of TNC inhibited the toll‑like receptor 4 (TLR4)/NF‑κB signaling pathway in PCOS rats and DHT‑treated KGN cells. In conclusion, knockdown of TNC could ameliorate PCOS in both rats and a cell model by inhibiting cell apoptosis, oxidative stress and inflammation via the suppression of the TLR4/NF‑κB signaling pathway.
摘要：
多囊卵巢综合征（PCOS）是育龄妇女中普遍存在的妇科疾病。本研究旨在探讨生腱蛋白C(TNC)在PCOS中的作用及其可能机制。空腹血糖和血清胰岛素，在PCOS大鼠中测定胰岛素抵抗的稳态模型评估和血清激素水平。此外,H&E染色用于评估病理学。此外,在PCOS大鼠和细胞模型中评估了TNC对氧化应激和炎症反应的影响.此外，采用EdU法和流式细胞术检测TNC对KGN细胞增殖和凋亡的影响。使用蛋白质印迹法测量TLR4/NF‑κB通路相关蛋白，免疫荧光和免疫组织化学。发现在PCOS大鼠和双氢睾酮（DHT）诱导的KGN细胞中mRNA和蛋白表达上调。敲除TNC减轻了PCOS大鼠的病理特征和内分泌异常。敲除TNC抑制卵巢细胞凋亡,PCOS大鼠的氧化应激和炎症反应。敲除TNC逆转了DHT诱导的KGN细胞增殖减少和凋亡增加。此外，抑制TNC减轻了DHT诱导的KGN细胞氧化应激和炎症反应。此外,TNC的敲除抑制PCOS大鼠和DHT处理的KGN细胞中的toll样受体4(TLR4)/NF‑κB信号通路。总之,敲除TNC可以通过抑制细胞凋亡改善大鼠和细胞模型的PCOS,氧化应激和炎症通过抑制TLR4/NF‑κB信号通路。
