触发AMPK-mTOR通路,调节与羊雷迪格细胞氧化应激相关的自
Liang Ma1, Kexin Li1, Yaru Guo1
1Laboratory of Animal Reproductive biotechnology, Shanxi Agricultural University, Taigu 030801, PR China.
Reproductive biology
|November 24, 2024
概括
过多的 (Se) 会诱导羊的莱迪格细胞的氧化应激,通过AMPK-mTOR通路触发自. 然而,适当的水平支持莱迪格细胞活力.
科学领域:
- 生殖生物学 生殖生物学
- 细胞应激反应的应激反应
- 微量元素的新陈代谢
背景情况:
- 莱迪格细胞对于男性生育至关重要,产生雄激素.
- 氧化应激会损害莱迪格细胞的功能和生存.
- 在莱迪格细胞生理学中的作用,特别是在压力下,需要进一步阐明.
研究的目的:
- 为了研究过度诱导的氧化应激对绵羊莱迪格细胞自的影响.
- 阐明潜在的分子机制,重点关注AMPK-mTOR途径.
主要方法:
- 羊的莱迪格细胞被分离出来,并用不同度的 (0.2.0,4.0,8.0μmol/L) 进行处理.
- 评估了细胞活力 (CCK-8测定),抗氧化剂状态 (ROS,GSH-Px) 和自标志物 (ATG5,LC3II/I).
- 评估了AMPK-mTOR通路激活 (西部斑块,实时PCR) 和C化合物的作用.
主要成果:
- 高 (8.0μmol/L) 降低了细胞活力,增加了ROS,降低了GSH-Px活性.
- 过量的提高了自标志物 (ATG5,LC3II/I),并激活了AMPK-mTOR通路.
- 化合物C抑制了AMPK-mTOR通路并减轻了诱导的自.
结论:
- 适当的 (2.0μmol/L) 增强了羊的莱迪格细胞活力.
- 过量的会诱导氧化应激,从而通过AMPK-mTOR通路激活自.
- 自-亡交叉影响莱迪格细胞命运,影响男性生育能力和精子生成.
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