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奎尔通过Nrf2-Keap1通路激活减轻了引起的急性肺损伤

Zhenjie Gao¹, Dadi Shu^2,3, Yuchen Li²

¹Engineering Research Center of Tropical Medicine Innovation and Transformation of Ministry of Education, School of Pharmacy, Hainan Medical University, Haikou, China.

Journal of biochemical and molecular toxicology

|August 28, 2025

概括

奎尔赛丁通过减少氧化应激和维护线粒体功能来防止诱导的急性肺损伤. 这种天然化合物显示了重金属暴露引起的肺损伤的治疗潜力.

科学领域:

毒理学毒理学毒理学
细胞生物学细胞生物学
生物化学生化学

背景情况:

暴露于会通过氧化应激和炎症引起肺组织损伤.
急性肺损伤 (ALI) 是一种严重的疾病,治疗选择有限.
了解防治毒性的保护机制至关重要.

研究的目的:

调查素对化 (CdCl2) 诱导的ALI的保护作用.
阐明奎尔丁作用的基本机制,重点关注氧化应激和线粒体通路.

主要方法:

已建立的CdCl2诱导ALI的老鼠和BEAS-2B细胞模型.
评估了细胞亡,增殖,炎症因子 (TNF-α,IL-6,IL-1β) 和氧化应激标志物.
使用的技术包括西斑,ELISA,流细胞计和CCK8测定.
研究了Nrf2-Keap1通路和线粒体功能.

主要成果:

奎尔在小鼠中显著降低了肺,组织损伤和炎症.
在肺细胞中抑制了亡,并在体外改善了细胞活力.
激活了Nrf2-Keap1信号通路,增加了抗氧化酶基因表达.
减少反应性氧物种 (ROS) 的产生和恢复氧化还原平衡.
保护了线粒体功能和膜潜力.

结论:

奎尔显示出对引起的急性肺损伤具有显著的保护作用.
该机制涉及减轻氧化应激和保护线粒体完整性.
奎尔素作为重金属引起的急性肺损伤的治疗剂具有潜力.

关键词:

肺部急性肺损伤是什么灭症 (apoptosis) 是一种死亡的过程.和是最重要的元素.氧化应激是一种氧化应激.文素 (Quercetin) 是一种文素.

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