Department of TCM Gynecology, Hunan Provincial Maternal and Child Health Care Hospital, Changsha, Hunan, P.R. China.
The Second Clinical College of Traditional Chinese Medicine, Hunan University of Chinese Medicine, Changsha, Hunan, P.R. China.
Gynecol Endocrinol. 2023 Dec;39(1):2223724. doi: 10.1080/09513590.2023.2223724. Epub 2023 Jun 19.
Polycystic ovary syndrome (PCOS) is a common endocrine disease in women of reproductive age, with complex pathological symptoms and mechanisms. This study explored the mechanism of action of Chao Nang Qing prescription (CNQP) in PCOS.
CNQP-medicated serum was prepared for culturing KGN granulosa cells. GATA3 knockdown, MYCT1 overexpression, and MYCT1 knockdown vectors were constructed to transfect KGN cells. Cell proliferation and apoptosis, as well as the expression of autophagy-related LC3-II/I, Beclin-1, and p62, were analyzed. ChIP was used to detect the binding of GATA3 and the MYCT1 promoter, and dual-luciferase reporter assay was used to analyze the influence of GATA3 on MYCT1 promoter activity.
CNQP treatment reduced proliferation, increased apoptosis, elevated LC3-II/I, Beclin-1, GATA3, and MYCT1 expression, and decreased p62 expression in KGN cells. GATA3 bound to the MYCT1 promoter to promote MYCT1 expression. MYCT1 overexpression impeded proliferation and stimulated apoptosis and autophagy in KGN cells. Compared to CNQP treatment alone, GATA3 or MYCT1 knockdown before CNQP treatment promoted proliferation and reduced apoptosis and autophagy in KGN cells.
CNQP may modulate KGN cell activity by upregulating GATA3 and MYCT1 expression, thereby slowing down the progression of PCOS.
多囊卵巢综合征（PCOS）是一种常见的育龄期女性内分泌疾病，具有复杂的病理症状和机制。本研究探讨了超脑清方（CNQP）在 PCOS 中的作用机制。
制备 CNQP 含药血清培养 KGN 颗粒细胞。构建 GATA3 敲低、MYCT1 过表达和 MYCT1 敲低载体转染 KGN 细胞。分析细胞增殖和凋亡以及自噬相关 LC3-II/I、Beclin-1 和 p62 的表达。ChIP 用于检测 GATA3 与 MYCT1 启动子的结合，双荧光素酶报告基因检测分析 GATA3 对 MYCT1 启动子活性的影响。
CNQP 处理降低了 KGN 细胞的增殖，增加了细胞凋亡，上调了 LC3-II/I、Beclin-1、GATA3 和 MYCT1 的表达，降低了 p62 的表达。GATA3 与 MYCT1 启动子结合，促进 MYCT1 的表达。MYCT1 过表达抑制 KGN 细胞的增殖并刺激其凋亡和自噬。与单独 CNQP 处理相比，在 CNQP 处理之前敲低 GATA3 或 MYCT1 促进了 KGN 细胞的增殖，减少了细胞凋亡和自噬。
CNQP 可能通过上调 GATA3 和 MYCT1 的表达来调节 KGN 细胞的活性，从而减缓 PCOS 的进展。
