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血纤维内克可以通过HUVEC的AMPK/Nrf2通路缓解由阿克罗林诱导的铁亡

Margaret Zaitoun¹, Yuandie Zhang², Fatqiatul Wulandari²

¹Department of Nutrition and Food Hygiene, Key Laboratory of Toxicology, School of Public Health, Key Laboratory of Public Health Safety and Emergency Prevention and Control Technology of Higher Education Institutions in Jiangsu Province, Nanjing Medical University, Nanjing, 211166, China; Faculty of Health Science, Homs University, Homs, Syria.

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

|June 5, 2025

概括

血纤维素素 (FN) 保护内皮细胞的亚克罗莱因诱导的铁亡. 这一发现揭示了FN FN.

科学领域:

生物化学生物化学
细胞生物学细胞生物学
毒理学毒理学毒理学

背景情况:

铁亡,一种被编程的细胞死亡,与心血管疾病等疾病有关.
一种环境污染物阿克罗莱因诱导铁灭菌.
血纤维素 (FN) 具有抗氧化和抗炎作用,但其对铁亡的作用尚不清楚.

研究的目的:

研究阿克罗莱因对人类静脉内皮细胞 (HUVECs) 铁亡的作用.
探索纤维素蛋白 (FN) 对抗阿克罗莱因诱导的铁亡的潜在保护作用.

主要方法:

在HUVEC中使用acrolein诱导ferroptosis.
对铁灭生物标志物的评估 (MDA,铁,ACSL4,TFRC,GPX4,SLC7A11).
评估纤维素蛋白的保护作用和潜在的信号通路 (AMPK/Nrf2).

主要成果:

在HUVEC中,阿克罗莱因诱导了铁,由增加的MDA,铁,ACSL4,TFRC和减少的GPX4,SLC7A11证明.
纤维肌菌素 (FN) 显著地保护了对阿克罗莱因诱导的铁死.
通过AMPK/Nrf2激活,FN减轻了脂质过氧化和炎症,通过AMPK/Nrf2激活逆转了ferroptosis生物标志物的变化.

结论:

纤维肌菌素 (FN) 在内皮细胞中表现出对烯蛋白诱导的铁亡的保护作用.
FN的保护机制包括激活AMPK/Nrf2通路,对GPX4和SLC7A11进行上调.
这项研究强调了FN作为减轻由阿克罗莱因诱导的内皮细胞损伤的潜在治疗点.

关键词:

亚克罗莱因是一种蛋白质.动脉样硬化是一种动脉样硬化.在HUVECEC中使用.血纤维素 (FN) 是一种

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