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通过ROS依赖途径诱导线粒细胞衰竭保护铜诱导的下丘脑神经细胞损伤

Song Zhu¹, Hongbin Wu², Hengmin Cui³

¹College of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu, 611130, China.

Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

|October 15, 2023

概括

高水平的硫酸铜损害了小鼠的下丘脑,导致氧化应激和线粒. 抗氧化剂如N-乙半氨酸 (NAC) 可能会防止铜诱导的神经毒性.

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:

铜 (Cu) 是必需的,但过量有毒,影响像大脑这样的器官.
铜诱导的下丘脑神经毒性的机制尚不清楚.
反应性氧物种 (ROS) 和线粒细胞衰变与细胞损伤有关.

研究的目的:

调查铜诱导的下丘脑神经毒性中ROS和线粒细胞衰变之间的联系.
探索线粒在防止铜诱导的下丘脑损伤中的作用.

主要方法:

用高硫酸铜 (CuSO4) 治疗的小鼠下丘脑.
评估了他的病理学变化,ROS产量和线粒的标志物 (LC3-II/LC3-I,p62).
评估了线粒体动力学 (MFN1,MFN2,DRP1,FIS1) 和ROS抑制剂 (NAC) 和线粒体抑制剂 (Mdivi-1) 的作用.

主要成果:

高CuSO4导致下丘脑神经元损伤,增加ROS,并诱导线粒.
CuSO4破坏了线粒体的融合/裂变平衡,增加了DRP1/FIS1和减少了MFN1/MFN2.
NAC降低了CuSO4诱导的线粒和正常化的线粒体动力学;Mdivi-1损害了细胞活力.

结论:

硫酸铜通过氧化应激诱导在下丘脑细胞和组织中的线粒细胞衰变.
线粒体的激活可能作为对铜诱导的线粒体功能障碍的保护机制.
这些发现为预防铜神经毒性提供了洞察力.

关键词:

SO () SO () SO () SO () SO () SO () SO () SO () SO () SO () SO () ) SO () SO () ) SO () SO () CuSO () SO () CuSO () ) CuSO ()脑下垂体的下垂体.线粒细胞衰变 - - 线粒细胞衰变 (mitophagy) 是一种鼠标鼠标是一个鼠标.这就是ROSOS ROS.

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