刺芒柄花素通过下调P53/SAT1/ACSL4介导的铁死亡改善新生小鼠缺氧缺血性脑损伤

doi:10.12122/j.issn.1673-4254.2026.03.14

南方医科大学学报 ›› 2026, Vol. 46 ›› Issue (3): 604-614.doi: 10.12122/j.issn.1673-4254.2026.03.14

• 基础研究 • 上一篇

刺芒柄花素通过下调P53/SAT1/ACSL4介导的铁死亡改善新生小鼠缺氧缺血性脑损伤

郭涛¹^,²(), 陈柏霖¹, 杨逍², 赵艳丽¹, 李晓敏¹, 何佳浩², 石金沙¹, 左涵珺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:2025-09-25 出版日期:2026-03-20 发布日期:2026-03-26
通讯作者: 李娟娟 E-mail:475612496@qq.com;lijuanjuan@kmmu.edu.cn
作者简介:郭涛，实验师，在读博士研究生，E-mail: 475612496@qq.com
基金资助:
国家自然科学基金(32460218);国家自然科学基金(31960194);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)

Formononetin downregulates P53/SAT1/ACSL4 pathway-mediated ferroptosis to improve hypoxic-ischemic brain injury in neonatal mice

Tao GUO¹^,²(), Bolin CHEN¹, Xiao YANG², Yanli ZHAO¹, Xiaomin LI¹, Jiahao HE², Jinsha SHI¹, Hanjun ZUO¹, 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:2025-09-25 Online:2026-03-20 Published:2026-03-26
Contact: Juanjuan LI E-mail:475612496@qq.com;lijuanjuan@kmmu.edu.cn
Supported by:
National Natural Science Foundation of China(32460218)

摘要/Abstract

摘要：

目的探讨刺芒柄花素（FMN）对新生小鼠缺氧缺血性脑损伤（HIBD）的神经保护作用，并阐明其机制是否与调控P53/SAT1/ACSL4信号通路以抑制神经元铁死亡有关。方法选取24只出生9~11 d的C57BL/6J新生小鼠，通过结扎左侧颈总动脉并置于低氧环境（92% N₂，8% O₂）中40 min以构建HIBD模型。造模成功后，将小鼠随机分为4组（n=6）：假手术组（Sham）、模型组（HIBD）、FMN低剂量治疗组（HIBD+FMN-L，50 mg/kg）和高剂量治疗组（HIBD+FMN-H， 100 mg/kg）。腹腔注射给药，3 d后取脑皮层缺血半暗带组织进行检测。采用Western blotting和双重免疫荧光技术分析铁死亡通路关键蛋白P53、SAT1及ACSL4的表达水平；同时测定组织内亚铁离子（Fe²⁺）、超氧化物（DHE）、丙二醛（MDA）和谷胱甘肽（GSH）的含量，以评估铁死亡及相关氧化应激指标。体外选用HT22神经元，建立氧糖剥夺（OGD）模型并分组为：对照组（Control）、模型组（OGD）、FMN干预组（OGD+FMN，100 μmol/L）、P53激动剂Nutlin-3干预组（OGD+Nutlin-3，10 μmol/L）以及FMN与Nutlin-3联合处理组（OGD+FMN+Nutlin-3）。在药物预处理1 h及OGD处理6 h后，检测上述铁死亡相关蛋白，并利用特异性探针或生化方法评估细胞内Fe²⁺（FerroOrange）、活性氧（DCFH-DA）、脂质过氧化（BODIPY-C11、MDA）、GSH水平、线粒体膜电位（JC-1）及细胞活性（CCK-8）。结果体内实验结果表明，与HIBD组相比，FMN治疗能够显著抑制P53、SAT1和ACSL4的蛋白表达（P<0.05），并有效改善铁死亡相关生化指标，具体为Fe²⁺、ROS和MDA含量显著降低，同时抗氧化物质GSH水平得以恢复（P<0.05）。体外实验结果与体内发现相互印证，FMN处理缓解了OGD诱导的HT22细胞铁死亡，表现为铁死亡关键蛋白表达下调（P<0.05），Fe²⁺积聚、脂质过氧化和ROS水平受到抑制，并且GSH含量、线粒体膜电位及细胞活力得到显著改善（P<0.05）。机制验证方面，当使用Nutlin-3特异性激活P53信号后，FMN所产生的上述保护效应均被明显逆转或削弱（P<0.05），P53信号在FMN抑制铁死亡过程中发挥重要的上游调节作用。结论刺芒柄花素通过下调P53/SAT1/ACSL4通路介导的神经元铁死亡的途径，对新生小鼠HIBD产生神经保护效应。

关键词: 刺芒柄花素, 缺氧缺血性脑损伤, 铁死亡, P53, SAT1, ACSL4

Abstract:

Objective To investigate the neuroprotective effects of formononetin (FMN) against hypoxic-ischemic brain damage (HIBD) in neonatal mice and the underlying mechanism. Methods Twenty-four neonatal C57BL/6J mice were randomly divided (n=6) into sham-operated group, HIBD model group, HIBD+FMN-L (50 mg/kg) group, and HIBD+FMN-H (100 mg/kg) group. Mouse models of HIBD were established by left common carotid artery ligation followed by hypoxia (92% N₂, 8% O₂) for 40 min. FMN at the two doses was administered by intraperitoneal injection, and 3 days later, brain tissues from the cortical ischemic penumbra were collected for assessing expressions of ferroptosis-related proteins (P53, SAT1, and ACSL4) using Western blotting and immunofluorescence staining and for detecting the levels of Fe²⁺, superoxide, malondialdehyde (MDA), and glutathione (GSH). In cultured HT22 neurons with oxygen-glucose deprivation (OGD), the effects of 100 μmol/L FMN, 10 μmol/L Nutlin-3 (a P53 agonist), or their combination on expressions of ferroptosis proteins, intracellular Fe²⁺, reactive oxygen species (ROS), lipid peroxidation, GSH, mitochondrial membrane potential, and cell viability were evaluated. Results In the neonatal mouse models of HIBD, FMN treatment significantly suppressed the protein expression of P53, SAT1, and ACSL4, reduced Fe²⁺, ROS, and MDA levels and increased GSH content in the cortical ischemic penumbra. In HT22 neurons with OGD, FMN obviously alleviated OGD-induced ferroptosis as shown by lowered expressions of the key ferroptosis proteins, reduced Fe²⁺ accumulation and lipid peroxidation, and significant increases of GSH levels, mitochondrial membrane potential, and cell viability. Mechanistic experiments showed that activation of P53 signaling by Nutlin-3 markedly reversed the protective effects of FMN. Conclusion FMN produces neuro-protective effects against HIBD in neonatal mice by mitigating neuronal ferroptosis, primarily through downregulation of the P53/SAT1/ACSL4 signaling pathway.

Key words: formononetin, hypoxic-ischemic brain damage, ferroptosis, P53, SAT1, ACSL4

郭涛, 陈柏霖, 杨逍, 赵艳丽, 李晓敏, 何佳浩, 石金沙, 左涵珺, 李娟娟. 刺芒柄花素通过下调P53/SAT1/ACSL4介导的铁死亡改善新生小鼠缺氧缺血性脑损伤[J]. 南方医科大学学报, 2026, 46(3): 604-614.

Tao GUO, Bolin CHEN, Xiao YANG, Yanli ZHAO, Xiaomin LI, Jiahao HE, Jinsha SHI, Hanjun ZUO, Juanjuan LI. Formononetin downregulates P53/SAT1/ACSL4 pathway-mediated ferroptosis to improve hypoxic-ischemic brain injury in neonatal mice[J]. Journal of Southern Medical University, 2026, 46(3): 604-614.

图/表 6

图1 FMN对HIBD后P53/SAT1/ACSL4铁死亡相关信号通路的影响

Fig.1 Effects of formononetin (FMN) on ferroptosis-related signaling pathways of P53/SAT1/ACSL4 in neonatal mice with HIBD. A: Western blotting bands of P53, SAT1, ACSL4 and β-actin. B-D: Statistical analysis of relative expressions of P53, SAT1 and ACSL4. *P<0.05, **P<0.01, ***P<0.001 (n=3).

图2 FMN对HIBD后P53及4-HNE在NeuN中荧光强度的变化

Fig.2 Effect of formononetin on fluorescence intensityof P53 and 4-HNE in the cortical ischemic penumbra of the mice with HIBD. A, B: Results of double immunofluorescence staining for P53 and NeuN (Scale bar=10 μm). C, D: Results of double immunofluorescence staining for 4-HNE and NeuN (Scale bar=10 μm). **P<0.01, ***P<0.001 (n=3).

图3 FMN对HIBD后Fe2+、DHE、MDA和GSH表达的影响

Fig.3 Effects of formononetin on Fe2+, DHE, MDA and GSH levels in the cortical ischemic penumbra of the mice with HIBD. A: Fe2+ levels in the 4 groups. B, C: Results of immunofluorescence staining for DHE (Scale bar=10 μm). D, E: Levels of MDA and GSH in the 4 groups. *P<0.05, **P<0.01, ***P<0.001 (n=3).

图4 FMN对神经元OGD后P53/SAT1/ACSL4铁死亡相关蛋白表达的影响

Fig.4 Effects of formononetin on expressions of P53, SAT1 and ACSL4 in HT22 neurons with oxygen-glucose deprivation (OGD). A-D: Western blotting for detecting expression levels of P53, SAT1 and ACSL4. E, F: Results of double immunofluorescence staining for P53 and NeuN (Scale bar=50 μm). *P<0.05, **P<0.01, ***P<0.001 (n=3).

图5 FMN对神经元OGD后Fe2+、DCFH-DA、BODIPY-C11、MDA和GSH表达的影响

Fig.5 Effects of formononetin on Fe2+, DCFH-DA, BODIPY-C11, MDA and GSH levels in HT22 neurons with OGD. A, B: Detection of Fe²⁺ levels using the FerroOrange fluorescent probe (Scale bar=10 μm). C, D: Detection of ROS levels using the DCFH-DA fluorescent probe (Scale bar=10 μm). E, F: Detection of lipid peroxidation using the BODIPY-C11 fluorescent probe (Scale bar=50 μm). G: Quantification of lipid peroxidation by MDA. H: Quantification of antioxidant products by GSH. *P<0.05, **P<0.01, ***P<0.001 (n=3).

图6 FMN对神经元OGD后的线粒体膜电位和细胞活力的影响

Fig.6 Effects of formononetin on mitochondrial membrane potential and cell viability in HT22 neurons with OGD. A, B: Representative images showing the JC-1 aggregates to monomers ratio for assessing mitochondrial membrane potential (Scale bar=50 μm). C: Assessment of HT22 cell viability by CCK-8 assay. *P<0.05, **P<0.01, ***P<0.001 (n=3).

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刺芒柄花素通过下调P53/SAT1/ACSL4介导的铁死亡改善新生小鼠缺氧缺血性脑损伤

Formononetin downregulates P53/SAT1/ACSL4 pathway-mediated ferroptosis to improve hypoxic-ischemic brain injury in neonatal mice

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