Tianjin Institute of Environmental and Operational Medicine, Tianjin, 300050, China.
Tianjin Institute of Environmental and Operational Medicine, Tianjin, 300050, China.
Biomed Pharmacother. 2020 Oct;130:110511. doi: 10.1016/j.biopha.2020.110511. Epub 2020 Jul 14.
Numerous studies have revealed that hypobaric hypoxia exposure elicited imbalance of homeostasis. However, the effects of intermittent hypobaric hypoxia (IHH) exposure on the female reproductive system have been rarely reported. This study aims to assess the effects of IHH on rat female reproductive system and explore the corresponding mechanism at the histological, endocrine and molecular levels.
The female rats were randomly divided into control and IHH groups. Multiple pathophysiological parameters, including body weight gain, organ coefficients, estrus cycle, and health signs were measured. Also, the reproductive hormones, hormone receptor mRNA expression and oxidant/antioxidant level were evaluated.
Significant increases of the heart, liver and lung coefficients were observed after IHH exposure. There were no statistically significant differences in ovarian and uterine coefficients, but changes were found in the morphology of the ovary and uterus. Additionally, the diestrus phase duration was significantly increased during IHH exposure. Furthermore, estrogen increased and the Luteinizing hormone and progesterone decreased after IHH exposure. Altered expression of ER, PR and LHR were also found in the IHH exposed rats. Importantly, IHH exposure significantly repressed the activities of GSH-Px and T-SOD and improved the contents of MDA.
Our results evince that IHH exposure caused estrus cycle irregularity. IHH induced oxidative stress along with ovarian and uterine structure damages, reproductive hormone disturbances and unusual expression of hormone receptors, thus suggesting a potential mechanism underlying IHH-induced reproductive system dysfunction.
大量研究表明,低压缺氧暴露会导致体内平衡失衡。然而,间歇性低压缺氧(IHH)暴露对女性生殖系统的影响却鲜有报道。本研究旨在评估 IHH 对雌性大鼠生殖系统的影响,并从组织学、内分泌和分子水平探讨其相应的机制。
将雌性大鼠随机分为对照组和 IHH 组。测量了多项生理病理参数,包括体重增加、器官系数、发情周期和健康状况。同时,评估了生殖激素、激素受体 mRNA 表达和氧化应激/抗氧化水平。
IHH 暴露后,心脏、肝脏和肺的系数显著增加。卵巢和子宫系数没有统计学差异,但卵巢和子宫的形态发生了变化。此外,IHH 暴露期间,发情间期持续时间显著增加。此外,雌激素增加,促黄体生成素和孕酮减少。在 IHH 暴露的大鼠中,还发现了 ER、PR 和 LHR 的表达改变。重要的是,IHH 暴露显著抑制了 GSH-Px 和 T-SOD 的活性,并提高了 MDA 的含量。
我们的结果表明,IHH 暴露导致发情周期不规则。IHH 诱导了氧化应激以及卵巢和子宫结构损伤、生殖激素紊乱和激素受体异常表达,提示 IHH 诱导生殖系统功能障碍的潜在机制。