五味子醇甲通过抑制ACSL4/TFRC/PTGS2信号通路缓解缺氧缺血性脑损伤小鼠神经元铁死亡

doi:10.12122/j.issn.1673-4254.2026.10.09

南方医科大学学报 ›› 2026, Vol. 46 ›› Issue (10): 2393-2404.doi: 10.12122/j.issn.1673-4254.2026.10.09

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五味子醇甲通过抑制ACSL4/TFRC/PTGS2信号通路缓解缺氧缺血性脑损伤小鼠神经元铁死亡

郭涛¹^,²(), 何佳浩², 董乐馨², 王朝¹, 左涵珺¹, 赵艳丽¹, 石金沙¹, 赵敏¹(), 李娟娟¹()

^1.昆明医科大学基础医学院人体解剖学与组织胚胎学系，云南昆明 650500
^2.昆明理工大学基础医学院解剖学教研室，云南昆明 650500

收稿日期:2026-03-23 出版日期:2026-10-20 发布日期:2026-10-26
通讯作者: 赵敏,李娟娟 E-mail:20190034@kust.edu.cn;zhaomin_kmmu@163.com;lijuanjuan@kmmu.edu.cn
作者简介:郭涛，实验师，在读博士研究生，E-mail: 20190034@kust.edu.cn
基金资助:
国家自然科学基金(32460218);国家自然科学基金(31960194);云南省科技厅基础研究计划基金(202401AY070001-069);昆明医科大学博士研究生创新基金(J114150330296);大学生创新训练计划基金(2024CYD038);大学生创新训练计划基金(S202410674118);大学生创新训练计划基金(S202510674161)

Schisandrin A alleviates neuronal ferroptosis in mice with hypoxic-ischemic brain injury by inhibiting the ACSL4/TFRC/PTGS2 signaling pathway

Tao GUO¹^,²(), Jiahao HE², Yuexin DONG², Zhao WANG¹, Hanjun ZUO¹, Yanli ZHAO¹, Jinsha SHI¹, Min ZHAO¹(), Juanjuan LI¹()

^1.Department of Human Anatomy & Histology and Embryology, School of Basic Medical Sciences, Kunming Medical University, Kunming 650500, China
^2.Department of Anatomy, School of Basic Medical Sciences, Kunming University of Science and Technology, Kunming 650500, China

Received:2026-03-23 Online:2026-10-20 Published:2026-10-26
Contact: Min ZHAO, Juanjuan LI E-mail:20190034@kust.edu.cn;zhaomin_kmmu@163.com;lijuanjuan@kmmu.edu.cn
Supported by:
National Natural Science Foundation of China(32460218)

摘要/Abstract

摘要：

目的研究五味子醇甲（Sch A）对缺氧缺血性脑损伤（HIBD）后神经元铁死亡的抑制作用，并阐明其机制是否与调控ACSL4/TFRC/PTGS2信号通路相关。方法体内实验选取36只出生后7~10 d的C57BL/6J新生小鼠，通过永久性结扎左侧颈总动脉并暴露于含8% O₂与92%N₂的低氧环境中持续40 min以制备HIBD模型。将小鼠随机分配至6组（6只/组）：假手术组（Sham）、模型组（HIBD）、Sch A低、中、高3个剂量组（HIBD+Sch A，10、30和90 mg/kg），以及铁死亡抑制剂组（HIBD+Fer-1，5 mg/kg）。连续给药3 d后，通过Western blotting检测脑皮层缺血半暗带组织中ACSL4、TFRC及PTGS2蛋白表达；免疫荧光染色观察ACSL4与4-HNE在神经元中的共定位情况；同时检测组织内活性氧（ROS）、丙二醛（MDA）、谷胱甘肽（GSH）及亚铁离子（Fe²⁺）水平。体外实验采用OGD诱导HT22神经元损伤，分为对照组（Control）、氧糖剥夺组（OGD）、Sch A干预组（OGD+Sch A，10 μmol/L）、ACSL4抑制剂PRGL493组（OGD+PRGL493，10 μmol/L）及联合干预组（OGD+Sch A+PRGL493）。药物预处理1 h及OGD处理6 h后，检测铁死亡相关蛋白表达、ROS生成、脂质过氧化（BODIPY-C11）、细胞活力（CCK-8）、线粒体膜电位（JC-1）、MDA、GSH及Fe²⁺水平。结果体内实验显示，HIBD后脑组织中ACSL4、TFRC、PTGS2表达显著上调（P<0.001），ACSL4与4-HNE在神经元中的共定位荧光强度明显增强，同时ROS、MDA及Fe²⁺水平升高，GSH含量下降（P<0.001）。Sch A干预后，上述变化均呈剂量依赖性逆转（P<0.05），效果与Fer-1相当。体外实验中，OGD诱导后神经元ACSL4、TFRC及PTGS2表达升高（P<0.001），ACSL4与NeuN共定位增强，ROS生成、脂质过氧化水平、MDA及Fe²⁺蓄积明显增加，GSH水平、细胞活力及线粒体膜电位下降（P<0.001）。Sch A或PRGL493单独干预均可改善上述指标（P<0.01），而二者联合应用后，ACSL4/TFRC/PTGS2蛋白表达进一步下调，氧化应激与脂质过氧化程度明显减轻，细胞活力及线粒体功能恢复更佳，Fe²⁺水平进一步降低（P<0.05）。结论五味子醇甲可通过抑制ACSL4/TFRC/PTGS2信号通路，减轻神经元铁死亡，从而对缺氧缺血性脑损伤发挥保护作用，其效应与铁死亡抑制剂Fer-1及ACSL4抑制剂PRGL493协同作用一致。

关键词: 五味子醇甲, 缺氧缺血性脑损伤, 铁死亡, 神经元, ACSL4/TFRC/PTGS2

Abstract:

Objective To investigate the inhibitory effect of schisandrin A (Sch A) on neuronal ferroptosis following hypoxic ischemic brain damage (HIBD) and the underlying mechanism. Methods Thirty-six neonatal C57BL/6J mice (7-10 days old) underwent sham operation (n=6) or permanent left carotid ligation followed by 40 min of hypoxic exposure and daily treatment with Sch A at 10, 30, or 90 mg/kg or with Fer 1 (5 mg/kg) for 3 consecutive days (n=6). Western blotting was used to detect protein expressions of ACSL4, TFRC, and PTGS2 in the cortical ischemic penumbra of the mice; ACSL4/4 HNE co localization in the neurons was detected by immunofluorescence staining, and the levels of ROS, MDA, GSH, and Fe²⁺ were quantified. In cultured HT22 hippocampal neurons with oxygen glucose deprivation (OGD), the effects of pretreatment (1 h prior to OGD) with Sch A (10 μmol/L) and PRGL493 (10 μmol/L), alone or in combination, were assessed by detecting expressions of ferroptosis related proteins, ROS production, lipid peroxidation, cell viability, mitochondrial membrane potential, and the levels of MDA, GSH, and Fe²⁺. Results In the neonatal mice, HIBD significantly upregulated ACSL4/TFRC/PTGS2, increased ACSL4/4 HNE co-localization and ROS, MDA, and Fe²⁺ levels, and decreased GSH in the cortical ischemic penumbra. Sch A dose-dependently reversed these changes with effects comparable to that of Fer-1. In cultured HT22 cells, OGD similarly upregulated these proteins, enhanced ACSL4/NeuN co-localization, increased ROS, lipid peroxidation, MDA, and Fe²⁺ levels, and reduced GSH, cell viability, and mitochondrial potential. Both Sch A and PRGL493 alone significantly ameliorated these changes, and their combined treatment further downregulated ACSL4, TFRC and PTGS2 expressions, more effectively alleviated oxidative stress and lipid peroxidation, restored cell viability and mitochondrial function, and reduced Fe²⁺ accumulation. Conclusion Sch A protects against HIBD in mice by inhibiting the ACSL4/TFRC/PTGS2 pathway and alleviating neuronal ferroptosis and produces synergistic effects with PRGL493.

Key words: schisandrin A, hypoxic-ischemic brain damage, ferroptosis, neurons, ACSL4/TFRC/PTGS2

郭涛, 何佳浩, 董乐馨, 王朝, 左涵珺, 赵艳丽, 石金沙, 赵敏, 李娟娟. 五味子醇甲通过抑制ACSL4/TFRC/PTGS2信号通路缓解缺氧缺血性脑损伤小鼠神经元铁死亡[J]. 南方医科大学学报, 2026, 46(10): 2393-2404.

Tao GUO, Jiahao HE, Yuexin DONG, Zhao WANG, Hanjun ZUO, Yanli ZHAO, Jinsha SHI, Min ZHAO, Juanjuan LI. Schisandrin A alleviates neuronal ferroptosis in mice with hypoxic-ischemic brain injury by inhibiting the ACSL4/TFRC/PTGS2 signaling pathway[J]. Journal of Southern Medical University, 2026, 46(10): 2393-2404.

图/表 6

图1 五味子醇甲对HIBD后铁死亡蛋白ACSL4/TFRC/PTGS2表达的影响

Fig.1 Effects of schisandrin A (Sch A) on expressions of ferroptosis-related proteins ACSL4, TFRC and PTGS2 in neonatal mice with hypoxic ischemic brain damage (HIBD). A: Western blotting of ACSL4, TFRC, and PTGS2 in the ischemic penumbra of the cerebral cortex of the neonatal mice in each group. B-D: Statistical analysis of the relative expression levels. ***P<0.001 vs Sham group; #P<0.05, ##P<0.01, ###P<0.001 vs HIBD group (n=3). L: Low; M: Medium; H: High; Fer-1: Ferrostatin-1.

图2 五味子醇甲对HIBD神经元ACSL4及4-HNE表达的影响

Fig.2 Effects of Sch A on expressions of ACSL4 and 4-HNE in brain neurons in mice with HIBD. A, D: Co-localization of ACSL4 or 4-HNE (red) with the neuronal marker NeuN (green) in the ischemic penumbra of the cerebral cortex detected by immunofluorescence double staining. B, C: Quantitative analysis of fluorescence intensity of ACSL4-NeuN and 4-HNE-NeuN. Scale bar=10 μm. ***P<0.001 vs Sham group; ##P<0.01, ###P<0.001 vs HIBD group (n=3).

图3 五味子醇甲对HIBD的氧化应激及铁过载的影响

Fig.3 Effects of Sch A on oxidative stress and iron overload following HIBD. A, B: ROS levels in the ischemic penumbra of mouse cerebral cortex detected by DHE fluorescence staining and quantitative analysis (Scale bar=10 μm). C: Relative expression levels of malondialdehyde (MDA). D: Relative expression levels of glutathione (GSH). E: Levels of ferrous ions (Fe²⁺). F: Ultrastructure of the neurons in the ischemic penumbra in each group observed by transmission electron microscopy (Original magnification: ×30 000; scale bar=500 nm). Red arrows indicate mitochondria. ***P<0.001 vs Sham group; #P<0.05, ##P<0.01, ###P<0.001 vs HIBD group (n=3).

图4 五味子醇甲联合ACSL4抑制剂PRGL493对OGD诱导神经元铁死亡的影响

Fig.4 Effects of Sch A combined with the ACSL4 inhibitor PRGL493 on OGD‑induced neuronal ferroptosis. A: Western blotting of ACSL4, TFRC, and PTGS2 protein expression levels in the neurons of each group. B-D: Statistical analysis of the relative expression levels of ACSL4, TFRC, and PTGS2 proteins. E, F: Immunofluorescence double staining for detecting co-localization of ACSL4 (red) with the neuronal marker NeuN (green). Scale bar=50 μm. ***P<0.001 vs Control group; ##P<0.01, ###P<0.001 vs OGD group; &P<0.05, &&&P<0.001 vs OGD+Sch A group (n=3). OGD: Oxygen-Glucose Deprivation.

图5 五味子醇甲对OGD诱导的神经元氧化应激及脂质过氧化的影响

Fig.5 Effects of Sch A on OGD induced neuronal oxidative stress and lipid peroxidation. A, B: ROS levels in the neurons detected by DCFH DA fluorescence staining. C, D: Oxidized/reduced lipid peroxidation levels in the neurons detected by BODIPY C11 fluorescence staining. E: Relative expression levels of MDA. F: Relative expression levels of GSH. Scale bar=50 μm. ***P<0.001 vs Control group; #P<0.05, ##P<0.01, ###P<0.001 vs OGD group; &P<0.05, &&P<0.01 vs OGD+Sch A group (n=3). MDA: Malondialdehyde; GSH: Glutathione.

图6 五味子醇甲对OGD诱导神经元活力、线粒体功能及铁积累的影响

Fig.6 Effects of Sch A on OGD induced neuronal viability, mitochondrial function, and iron accumulation. A: Neuronal viability detected by CCK-8 assay. B, C: Fluorescence staining of mitochondrial membrane potential detected by JC-1 staining. D, E: Neuronal iron ion levels detected by Fe²⁺ fluorescence staining. Scale bar=50 μm. ***P<0.001 vs Control group; #P<0.05, ##P<0.01, ###P<0.001 vs OGD group; &P<0.05, &&P<0.01 vs OGD+Sch A group (n=3).

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五味子醇甲通过抑制ACSL4/TFRC/PTGS2信号通路缓解缺氧缺血性脑损伤小鼠神经元铁死亡

Schisandrin A alleviates neuronal ferroptosis in mice with hypoxic-ischemic brain injury by inhibiting the ACSL4/TFRC/PTGS2 signaling pathway

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