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抑制Nrf2活动,缓解诱导的线粒体损伤和热死

Hao Xu^1,2, Jingyi Yang^1,2, Ruiqi Ye^1,2

¹College of Animal Science, Anhui Science and Technology University, Fengyang, 233100, China.

Biological trace element research

|August 9, 2025

概括

暴露于会通过破坏线粒体和增加氧化应激,激活NLRP3炎症酶和火死,导致肝损伤. 抗氧化剂可以防止这种重金属毒性.

科学领域:

毒理学毒理学毒理学
细胞生物学细胞生物学
免疫学免疫学免疫学

背景情况:

急性 (Cd) 暴露会通过氧化应激和炎症引起肝损伤.
在肝脏疾病中,NLRP3炎症酶与激素灭亡,一种编程细胞死亡形式有关.
诱导的肝细胞损伤的机制尚未完全理解.

研究的目的:

研究对小鼠肝细胞 (BNL CL.2细胞) 的细胞毒性作用.
阐明引起的肝损伤背后的分子机制.
探索氧化应激和NLRP3炎症酶在毒性的作用.

主要方法:

BNL CL.2 细胞的Cd 暴露.
评估线粒体功能,活性氧物种 (ROS) 水平和NLRP3炎症酶激活.
评估火性特征和Nrf2转录活性.
干预ROS清洁者N-乙半氨酸 (NAC) 和Mito-TEMPO的干预.

主要成果:

暴露于Cd诱导了线粒体功能障碍和肝细胞中过度的ROS产生.
Cd触发了NLRP3炎症酶激活和烧灭,由血膜破裂证明.
NAC和Mito-TEMPO减轻了Cd引起的损害,突出了ROS的关键作用.
Cd抑制了Nrf2活性,损害了抗氧化防御,破坏了氧化还原平衡.

结论:

通过线粒体损伤,ROS生成和NLRP3炎症酶激活诱导肝细胞烧灭.
Nrf2通路的破坏通过破坏抗氧化剂反应,有助于的肝毒性.
红色氧化物是引起的肝损伤的关键媒介,表明潜在的治疗点.

关键词:

是的组成部分.线粒体损伤导致线粒体损伤.在NLRP3炎症酶体中,NLRP3炎症 Nrf2 信号通道的信号通道热灭菌的发生.

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