摘要： 目的 分析高盐饮食对卵巢线粒体功能的影响。方法 将20只雌性ICR小鼠随机分为正常盐饮食（NSD）组和高盐饮食（HSD）组，每组10只。NSD组给予正常盐饮食，HSD组给予8% NaCl高盐饮食，持续4周。通过NaCl诱导体外培养的人卵巢颗粒细胞COV-434建立高盐处理细胞模型。采用Western blotting检测超氧化物歧化酶（SOD）和电子传递链复合物（Complex） Ⅰ~Ⅴ的表达情况，动力学法检测SOD和琥珀酸脱氢酶（SDH）的活性，化学发光法检测ATP水平。结果 与NSD组相比，HSD组小鼠卵巢Complex Ⅰ表达水平显著下降（P < 0.01），Complex Ⅴ表达水平显著升高（P < 0.05），SDH活性显著降低（P < 0.01），血清和卵巢中ATP含量也显著下降（P < 0.01）。高盐处理后COV-434细胞中Complex Ⅰ和Complex Ⅱ表达水平显著下降（P < 0.05），Complex Ⅴ表达水平显著升高（P < 0.05），SDH活性显著降低（P < 0.01），ATP含量不足（P < 0.01）。结论 高盐可引起小鼠卵巢线粒体的氧化稳态失衡、Complex表达水平变化、三羧酸循受阻以及ATP水平不足等线粒体功能障碍。

高盐饮食导致小鼠卵巢组织线粒体功能异常

侯恩太^1,2,3,4, 顾晓阳^1,2,3,4, 倪士峰⁵, 李新宇^1,2,3,4, 乔杰^1,2,3,4

1. 北京大学第三医院妇产科生殖医学中心, 北京 100191;
2. 国家妇产科疾病临床医学研究中心 (北京大学第三医院), 北京 100191;
3. 辅助生殖教育部重点实验室 (北京大学), 北京 100191;
4. 北京市生殖内分泌与辅助生殖技术重点实验室, 北京 100191;
5. 西北大学生命科学学院中药系, 西安 710069

收稿日期:2023-07-20出版日期:2024-02-28发布日期:2024-01-12
通讯作者:乔杰E-mail:jie.qiao@263.net
作者简介:侯恩太(1986-),男,助理研究员,博士.
基金资助:国家自然科学基金（82103106）


关键词: 高盐饮食, 小鼠卵巢, 线粒体功能障碍, 电子传递链, 琥珀酸脱氢酶
Abstract: Objective To analyze the effect of a high salt diet on ovarian mitochondrial function. Methods Twenty female ICR mice were randomly divided into a normal salt diet (NSD) group and a high salt diet (HSD) group (n=10 each). The NSD group was given a normal salt diet and the HSD group was given an 8% NaCl diet for 4 weeks. A high salt-treated cell model was established by inducing COV-434 cells cultured in vitro with NaCl. Western blotting was used to detect the protein expression of superoxide dismutase (SOD) and ComplexesⅠ-Ⅴ. The activity of SOD and succinate dehydrogenase (SDH) was detected kinetically. A chemiluminescence assay was used to detect adenosine triphosphate (ATP) levels. Results Compared with the NSD, the HSD significantly reduced the expression level of ComplexⅠin ovarian mitochondria (P < 0.01), significantly increased the expression level of ComplexⅤ (P < 0.05), and significantly reduced the activity of SDH and content of ATP (P < 0.01). The expression level of ComplexesⅠandⅡdecreased significantly (P < 0.05), expression level of ComplexⅤ increased significantly (P < 0.05), activity of SDH decreased significantly (P < 0.01), and content of ATP was insufficient (P < 0.01) in COV-434 cells cultured under high salt conditions. Conclusion High salt can lead to mitochondrial dysfunction in the mouse ovary, such as imbalanced oxidative homeostasis, changed expression level of electron transport chain complexes, blocked tricarboxylic acid cycle, and insufficient ATP level.
Key words: high salt diet, mouse ovary, mitochondrial dysfunction, electronic transfer chain, succinate dehydrogenase
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