补充铜可以缓解缺氧诱导的铁和神经元细胞中氧化应激
Jianyu Wang1, Yuankang Zou1, Ruili Guan1
1Department of Occupational and Environmental Health and the Ministry‑of‑Education's Key Laboratory of Hazard Assessment and Control in Special Operational Environment, School of Preventive Medicine, Fourth Military Medical University, Xi'an, Shaanxi 710032, P.R. China.
International journal of molecular medicine
|October 18, 2024
概括
补充铜可以保护新生儿的大脑细胞免受缺氧损伤. 它通过增强超氧化脱酶/SOD1/谷氨过氧化酶4通路的铜陪伴剂来减轻氧化应激和铁亡,改善细胞活力.
科学领域:
- 神经科学是一个神经科学.
- 细胞生物学 细胞生物学
- 生物化学 生物化学
背景情况:
- 缺氧性缺血是新生儿脑损伤的主要原因.
- 铜在缺血性脑损伤中的保护机制尚未完全理解.
研究的目的:
- 研究铜如何在神经元细胞模型中减轻缺氧诱导的氧化应激和铁亡.
- 为了阐明参与铜神经保护作用的潜在分子通路.
主要方法:
- 建立了一个缺氧HT22细胞模型.
- 评估了细胞活力,线粒体结构,活性氧物种,脂质过氧化和细胞内铜水平.
- 分析了关键氧化应激和铁灭菌标记的基因和蛋白质表达,包括超氧化脱氧化酶/SOD1/氨酸过氧化酶4轴的铜伴侣.
主要成果:
- 缺氧降低了细胞活力,增加了铁亡的标志物,氧化应激 (ROS,H2O2,MDA) 和降低了超氧化物解酶1 (SOD1) 活性.
- 在低氧条件下,细胞内铜水平下降.
- 铜补充剂使细胞活力正常化,减少了氧化应激和铁亡,并对超氧化脱氧化酶/SOD1/谷氨酸过氧化酶4通路的铜伴侣进行了上调.
结论:
- 铜在神经元中起着新的保护作用,防止缺氧诱导的氧化应激和铁亡.
- 补充铜显示治疗潜力减轻神经元损伤在低氧条件下.
相关概念视频
01:16Necrosis
4.4K
Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become...
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become...
4.4K
01:46Electron Transport Chain: Complex I and II
12.0K
The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
ROS generation is regulated and maintained at moderate levels necessary...
12.0K