Department of Gynecology, Guangdong Women and Children Hospital, 511400, China.
Department of Obstetrics and Gynecology, Nanfang Hospital, Southern Medical University, Guangzhou 510000, China.
Biomed Res Int. 2022 Jul 7;2022:3862122. doi: 10.1155/2022/3862122. eCollection 2022.
Premature ovarian failure refers to a series of symptoms of perimenopausal hot flashes, night sweats, decreased libido, vaginal dryness, insomnia, reduced menstruation, sparse hair, even amenorrhea, and even infertility before the age of 40 due to the decline of ovarian function. Premature ovarian failure is a common and difficult disease in gynecology. Its prevalence is increasing gradually, and the trend is younger. The aim of this experiment was to elucidate the role of human umbilical cord mesenchymal stem cells (HUCMSCs) in premature ovarian failure and its mechanism. HUCMSCs, KGN cells, and HEK293T cells were used in this experiment. Quantitative PCR and microarray analysis, ELISA inflammation and oxidative stress kits, RNA pull-down assay, luciferase reporter assay, proliferation assay, EDU staining, and Western blot analysis were used. In an in vitro model of premature ovarian failure, HUCMSCs attenuated inflammatory response, oxidative stress, and apoptosis. HUCMSCs ameliorated the premature ovarian failure model. The miR-100-5p expression was induced by HUCMSCs through methylation. miR-100-5p regulation influenced the role of HUCMSCs in an in vitro model of premature ovarian failure. HUCMSCs inhibited the in vitro expression of NOX4, NLRP3, and GSDMD proteins in the model. NOX4/NLRP3 signaling pathway affects the role of HUCMSCs in an in vitro model of premature ovarian failure through miR-100-5p. This experiment elucidated the role of HUCMSCs in premature ovarian failure and its mechanism, with a view to providing a clinical reference.
卵巢早衰是指由于卵巢功能衰退而导致 40 岁之前出现一系列围绝经期症状，如烘热汗出、性欲减退、阴道干涩、失眠、月经减少、毛发稀疏，甚至闭经、不孕等，是妇科常见而又难治的疾病之一。其发病率逐渐增高，且呈年轻化趋势。本实验旨在探讨人脐带间充质干细胞（HUCMSCs）在卵巢早衰中的作用及其机制。本实验使用 HUCMSCs、KGN 细胞和 HEK293T 细胞。采用定量 PCR 和微阵列分析、ELISA 炎症和氧化应激试剂盒、RNA 下拉测定、荧光素酶报告测定、增殖测定、EDU 染色和 Western blot 分析。在卵巢早衰的体外模型中，HUCMSCs 减弱了炎症反应、氧化应激和细胞凋亡。HUCMSCs 改善了卵巢早衰模型。HUCMSCs 通过甲基化诱导 miR-100-5p 的表达。miR-100-5p 的调节影响了 HUCMSCs 在卵巢早衰体外模型中的作用。HUCMSCs 抑制了模型中 NOX4、NLRP3 和 GSDMD 蛋白的体外表达。NOX4/NLRP3 信号通路通过 miR-100-5p 影响 HUCMSCs 在卵巢早衰体外模型中的作用。本实验阐明了 HUCMSCs 在卵巢早衰中的作用及其机制，以期为临床提供参考。
