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α-亚麻酸通过激活Nrf2抑制铁死亡，从而预防中暑诱导的急性肺损伤。

Alpha-linolenic acid protects against heatstroke-induced acute lung injury by inhibiting ferroptosis through Nrf2 activation.

作者信息

Wang Lin, Ma Jiamin, Li Zhaozheng, Zhao Xinru, Chen Ying, Wang Pei, Li Yi, Chen Yuwei, Yao Xuanqi, Yao Liangfang, Li Jinbao

机构信息

School of Anesthesiology, Shandong Second Medical University, Weifang, People's Republic of China.

Department of Anesthesiology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.

出版信息

Redox Rep. 2025 Dec;30(1):2538294. doi: 10.1080/13510002.2025.2538294. Epub 2025 Jul 27.

DOI:10.1080/13510002.2025.2538294
PMID:40717294
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12305878/
Abstract

Heatstroke (HS)-induced acute lung injury (ALI) has high morbidity and mortality with no specific therapies. Ferroptosis, a form of programmed cell death driven by lipid peroxidation due to reduced Glutathione Peroxidase 4 (GPX4) activity, is closely linked to HS-induced ALI. This study investigated the effect of alpha-linolenic acid (ALA), a plant-derived ω-3 fatty acid, on ferroptosis in a mouse model of HS-induced ALI. Histopathology analysis found that ALA can attenuate lung injury and improve the 7-day survival rate in mice with HS-induced ALI. In addition, ALA significantly reduced the levels of reactive oxygen species (ROS) and malondialdehyde (MDA), while increasing the level of antioxidant glutathione (GSH). Further analysis showed that ALA upregulated the levels of SLC7A11 and GPX4 by promoting the nuclear translocation of Nrf2. This led to increased GSH synthesis but reduced ROS accumulation, which in turn suppressed ferroptosis and protected the mice against HS-induced ALI. Additionally, the protective effect of ALA was found to be diminished in -deficient mice. In summary, ALA inhibits ferroptosis in macrophages by activating the Nrf2/SLC7A11/GPX4 pathway and attenuates HS-induced ALI.

摘要

中暑（HS）诱导的急性肺损伤（ALI）发病率和死亡率高，且没有特异性治疗方法。铁死亡是一种由于谷胱甘肽过氧化物酶4（GPX4）活性降低导致脂质过氧化驱动的程序性细胞死亡形式，与HS诱导的ALI密切相关。本研究调查了植物来源的ω-3脂肪酸α-亚麻酸（ALA）对HS诱导的ALI小鼠模型中铁死亡的影响。组织病理学分析发现，ALA可减轻HS诱导的ALI小鼠的肺损伤并提高其7天生存率。此外，ALA显著降低了活性氧（ROS）和丙二醛（MDA）水平，同时提高了抗氧化剂谷胱甘肽（GSH）水平。进一步分析表明，ALA通过促进Nrf2的核转位上调了SLC7A11和GPX4的水平。这导致GSH合成增加但ROS积累减少，进而抑制铁死亡并保护小鼠免受HS诱导的ALI。此外，发现ALA在Nrf2缺陷小鼠中的保护作用减弱。总之，ALA通过激活Nrf2/SLC7A11/GPX4途径抑制巨噬细胞中的铁死亡，并减轻HS诱导的ALI。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/142e/12305878/053ae03c8349/YRER_A_2538294_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/142e/12305878/f23894fbca38/YRER_A_2538294_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/142e/12305878/c7cb94630860/YRER_A_2538294_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/142e/12305878/cb5dff0a88ca/YRER_A_2538294_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/142e/12305878/cf94f0e50765/YRER_A_2538294_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/142e/12305878/e6e3b0e82b03/YRER_A_2538294_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/142e/12305878/ebdff5ac7cb5/YRER_A_2538294_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/142e/12305878/053ae03c8349/YRER_A_2538294_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/142e/12305878/f23894fbca38/YRER_A_2538294_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/142e/12305878/c7cb94630860/YRER_A_2538294_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/142e/12305878/cb5dff0a88ca/YRER_A_2538294_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/142e/12305878/cf94f0e50765/YRER_A_2538294_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/142e/12305878/e6e3b0e82b03/YRER_A_2538294_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/142e/12305878/ebdff5ac7cb5/YRER_A_2538294_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/142e/12305878/053ae03c8349/YRER_A_2538294_F0007_OC.jpg

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本文引用的文献

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Insights into pathophysiology and therapeutic strategies for heat stroke: Lessons from a baboon model.中暑病理生理学和治疗策略的新见解：狒狒模型的启示。
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Ferroptosis turns 10: Emerging mechanisms, physiological functions, and therapeutic applications.铁死亡研究十周年：新兴机制、生理功能与治疗应用
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