慢性不可预测的压力会引发类似焦虑的行为和氧化压力,导致卵巢储备减少
Zhihao Zhou1,2, Yangshuo Li1, Jie Ding1
1Department of Traditional Chinese Gynecology, The First Affiliated Hospital of Naval Military Medical University (Changhai Hospital), 168 Changhai Road, Yangpu District, Shanghai, China.
Scientific reports
|December 27, 2024
概括
慢性压力会损害卵巢储备,因为它会损害粒状细胞并减少ATP的产生. 这项研究揭示了新动物模型中压力诱导的卵巢储量减少 (DOR) 背后的氧化应激机制.
科学领域:
- 生殖内分泌学 生殖内分泌学
- 细胞生物学 细胞生物学
- 压力生理学 压力生理学
背景情况:
- 慢性压力对女性生殖内分泌系统产生负面影响,可能导致卵巢功能障碍.
- 现有的研究尚未完全阐明压力诱导的卵巢损伤的生化途径.
- 更深入地了解这些机制对于解决卵巢储量减少 (DOR) 至关重要.
研究的目的:
- 建立一种可靠的动物模型,用于慢性不可预测压力 (CUS) 引起的DOR.
- 研究CUS诱导的卵巢损伤背后的生物化学和细胞机制.
- 确定关键的分子事件,将CUS与卵巢储备受损联系起来.
主要方法:
- 在八周内建立了一种慢性不可预测压力 (CUS) 鼠标模型.
- 评估卵巢功能标志物,包括卵泡计数,AMH,FSH和皮质水平.
- 分析了卵巢ATP新陈代谢,氧化应激标志物和粒粉细胞亡.
- 研究了线粒体通路在CUS诱导的粒状细胞亡中的作用.
主要成果:
- CUS显著增加毛囊缩,AMH降低,FSH水平升高.
- 在血液和卵巢组织中观察到高水平的皮质.
- 检测到卵巢ATP代谢异常和氧化应激增加.
- 通过线粒体通路,CUS在小鼠卵巢颗粒细胞 (mGCs) 中诱导了亡,这与ATP生产减少有关.
结论:
- 在mGC中,CUS通过氧化应激和亡诱导DOR,主要是通过破坏ATP代谢.
- 在mGC中ATP产量的减少是CUS诱导DOR的关键指标.
- 已建立的CUS模型为进一步研究与压力相关的生殖障碍提供了一个平台.
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