暴露于会通过mtROS-ferritinophagy通路诱导神经元铁亡和认知缺陷
Dongmei Wang1, Yiran Wu1, Xiang Zhou1
1College of Basic Medicine and Forensic Medicine, Henan University of Science and Technology, Luoyang, China.
Environmental pollution (Barking, Essex : 1987)
|April 15, 2024
概括
环境中的暴露会引起神经毒性和认知衰退,因为它会诱导细胞死亡的一种类型 - - 铁亡. 自和线粒体的活性氧物种是引起的神经元损伤的关键媒介.
科学领域:
- 神经科学是一个神经科学.
- 毒理学 毒理学 毒理学
- 细胞生物学 细胞生物学
背景情况:
- 环境中的 (Cd) 暴露与神经元死亡和认知障碍有关.
- 铁,一种依赖于铁的调节细胞死亡形式,在神经系统疾病中起作用.
研究的目的:
- 为了研究铁灭菌在引起的神经毒性的作用.
- 阐明海马神经元中诱导的铁死背后的机制.
主要方法:
- 在小鼠海马和HT22神经元细胞系中暴露Cd.
- 评估ferroptotic标记物,细胞内铁和脂质过氧化.
- 操纵自 (使用3-MA和CQ) 和NCOA4表达.
- 在体内通过ferrostatin-1 (Fer-1) 抑制ferroptosis.
主要成果:
- 暴露于CD诱导了海马神经元中的铁亡,以增加的铁亡标记物,铁和脂质过氧化为证.
- 自抑制改善了Cd诱导的铁亡.
- 通过NCOA4介导的费里丁降解对Cd诱导的费洛症至关重要.
- 线粒体反应性氧物种 (mtROS) 对于铁素代介导的铁死是必不可少的.
- 铁素-1治疗保护了Cd诱导的神经元死亡和认知缺陷.
结论:
- 铁亡是一种新的机制,有助于Cd诱导的神经毒性和认知障碍.
- mtROS-ferritinophagy通路是Cd诱导的神经元铁亡的一个关键调节器.
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