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铜缺乏症诱导小鼠肝脏的氧化应激通过阻断Nrf路径

Zhiying Pan¹, Chengfeng Deng¹, Lian Shui¹

¹Sichuan Mianyang 404 Hospital, Mianyang, 621010, Sichuan, People's Republic of China.

Biological trace element research

|July 12, 2023

概括

缺乏铜会通过增加氧化应激和抑制Nrf2通路来损害肝脏. 补充硫酸铜 (CuSO4) 在小鼠中逆转了这些有害影响.

科学领域:

生物化学生物化学
肝病学肝病学是一种肝病学.
营养科学营养科学

背景情况:

铜 (Cu) 对许多生理过程和金属蛋白合成至关重要.
肝脏是铜代谢和金属蛋白生产的主要器官.

研究的目的:

为了研究铜缺乏对肝脏健康的影响.
评估肝脏氧化应激的变化,阐明潜在的机制.

主要方法:

给小鼠食缺乏铜的饮食.
铜缺乏症通过腹膜内硫酸铜 (CuSO4) 注射来纠正.
分析了肝脏指数,组织学,血清生物化学和Nrf2通路标记物.

主要成果:

铜缺乏导致肝脏指数下降,组织学损伤和氧化应激增加.
血清ALT和AST水平升高,而肝铜和ALB含量下降.
Nrf2通路分子 (Nrf2,HO-1,NQO1) 减少,而Keap1增加.
硫酸铜补充剂改善了这些不良影响.

结论:

铜缺乏导致小鼠的肝损伤.
这种损伤与氧化应激激活和Nrf2通路抑制有关.
补充铜可以减轻铜缺乏引起的肝损伤.

关键词:

铜缺乏症铜缺乏症肝脏肝脏肝脏肝脏鼠标鼠标是一个鼠标.Nrf2 路径的路径氧化应激是一种氧化应激.

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