Jiajia Duan, Yiping Wang, Enyan Jiang, Shouwu Zhu, Shuai Yang, Xiaojian Zhang, Juan Jiang, Zhen Fang, Jia Zeng, Jikai Wang, Yang Yan, Huiqing Li, Fei Liu
Department of Neurosurgery, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, Guangdong 519000, China; Guangdong Engineering Research Center of Molecular Imaging, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai 519000, Guangdong, China.
Department of Radiotherapy, The Cancer Center of The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, Guangdong 519000, China.
Exp Neurol. 2025 Jul;389:115258. doi: 10.1016/j.expneurol.2025.115258. Epub 2025 Apr 14.
Ferroptosis plays a critical role in radiation-induced brain injury (RIBI). The role of Maresin-1, which has anti-inflammatory and antiferroptotic properties, in RIBI is still unclear. This study aimed to explore the effects and mechanisms of Maresin-1 on ferroptosis after RIBI in mice. A mouse model of RIBI was constructed through whole-brain irradiation. Short-term neurological functions were evaluated by the modified Garcia score and the beam balance score, and long-term neurological functions were evaluated by the Morris water maze and the rotarod test. Changes in the number of NeuN-positive neurons were detected through immunohistochemistry. The lipid peroxidation level was evaluated by detecting the contents of malondialdehyde (MDA), 4-hydroxynonenal (4-HNE), glutathione-reduced (GSH) and glutathione-oxidized (GSSG). The expression of the ferroptosis-related markers glutathione peroxidase 4 (GPX4) and cyclooxygenase 2 (COX2) was assessed via Western blotting. Adeno-associated viruses were used to knock down retinoic acid receptor-related orphan receptor alpha (RORα) or nuclear factor erythroid 2-related factor 2 (NRF2) to explore the mechanism by which Maresin-1 alleviates ferroptosis. The results showed that Maresin-1 could significantly reduce the levels of MDA, 4-HNE, GSSG, and COX2 after RIBI; increase the contents of GSH and GPX4; reduce neuronal loss in the cortex and hippocampus; and improve the short-term and long-term neurological functions of mice. After the knockdown of RORα or NRF2, the protective effects of Maresin-1 in mediating anti-lipid peroxidation and anti-ferroptosis were abolished. Our study revealed that Maresin-1 partially alleviates lipid peroxidation-induced ferroptosis after RIBI in mice via the RORα and NRF2 pathways, improving their neurological functions. This study highlights the protective role of Maresin-1 in RIBI and provides a feasible therapeutic strategy for subsequent in-depth research and clinical intervention.
铁死亡在辐射诱导的脑损伤(RIBI)中起关键作用。具有抗炎和抗铁死亡特性的maresin-1在RIBI中的作用仍不清楚。本研究旨在探讨maresin-1对小鼠RIBI后铁死亡的影响及机制。通过全脑照射构建RIBI小鼠模型。采用改良Garcia评分和平衡木评分评估短期神经功能,采用Morris水迷宫和转棒试验评估长期神经功能。通过免疫组织化学检测NeuN阳性神经元数量的变化。通过检测丙二醛(MDA)、4-羟基壬烯醛(4-HNE)、还原型谷胱甘肽(GSH)和氧化型谷胱甘肽(GSSG)的含量评估脂质过氧化水平。通过蛋白质免疫印迹法评估铁死亡相关标志物谷胱甘肽过氧化物酶4(GPX4)和环氧化酶2(COX2)的表达。使用腺相关病毒敲低视黄酸受体相关孤儿受体α(RORα)或核因子红细胞2相关因子2(NRF2),以探讨maresin-1减轻铁死亡的机制。结果表明,maresin-1可显著降低RIBI后MDA、4-HNE、GSSG和COX2的水平;增加GSH和GPX4的含量;减少皮质和海马区的神经元丢失;并改善小鼠的短期和长期神经功能。敲低RORα或NRF2后,maresin-1介导的抗脂质过氧化和抗铁死亡的保护作用消失。我们的研究表明,maresin-1通过RORα和NRF2途径部分减轻小鼠RIBI后脂质过氧化诱导的铁死亡,改善其神经功能。本研究突出了maresin-1在RIBI中的保护作用,为后续深入研究和临床干预提供了可行的治疗策略。