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甲基氨酸提升Nrf2-GPX4轴缓解内皮功能障碍和暴露诱导的铁亡

Zhihui Cai¹, Yutian Zhang¹, Leting He¹

¹Department of Health Management of the Guangdong Second Provincial General Hospital & Postdoctoral Research Station of Basic Medicine of the School of Medicine; Department of Bioscience and Biotechnology of the College of Life Science and Technology, Jinan University, Guangzhou 510317, China.

Journal of agricultural and food chemistry

|March 12, 2025

概括

长期暴露于会通过诱导内皮铁死来损害心血管健康. 补充剂,特别是甲基酸 (MSA),通过向Se-Nrf2/GPX4通路来减轻这种损害,提供了一个潜在的治疗策略.

科学领域:

环境健康环境健康
毒理学毒理学毒理学
心血管生物学心血管生物学

背景情况:

慢性 (As) 暴露与心血管疾病有关.
铁亡,一种涉及 (Se) 的细胞死亡途径,与As的毒性有关.
Se在通过铁死来抵消As诱导的内皮功能障碍中的作用尚未完全理解.

研究的目的:

研究Se补充剂对As诱导的内皮功能障碍的保护作用和机制.
探索铁化对As毒性的参与以及甲基烯酸 (MSA) 的潜在缓解.

主要方法:

使用小鼠和小鼠大动脉内皮细胞的体内和体外研究.
评估内皮功能障碍标志物 (透性,循环细胞,线粒体变化).
评估了铁,氧化还原稳定,Se状态和蛋白表达 (GPX4),包括Nrf2通路激活.

主要成果:

暴露导致内皮功能障碍和ferroptosis在体内和体外.
在As暴露的细胞中观察到受损的还原氧平衡,降低的Se状态和降低的GPX4表达.
甲基烯酸 (MSA) 治疗通过激活Nrf2和升调GPX4异型减弱了As诱导的铁和功能障碍.

结论:

通过破坏Se-Nrf2/GPX4轴诱导内皮铁和功能障碍.
甲基烯酸 (MSA) 通过减轻铁亡,显示出对As诱导的内皮损伤的保护作用.
这项研究强调了在保护心血管系统免受毒性的关键作用.

关键词:

在GPX4中使用GPX4.Nrf2 没有任何问题.亚是一种.内皮质功能障碍在内皮质功能障碍铁性化 (ferroptosis) 是一种是一种.

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