miR-24-3p靶向GSK-3β抑制铁死亡促进大鼠脊髓损伤修复

doi:10.12122/j.issn.1673-4254.2026.04.01

南方医科大学学报 ›› 2026, Vol. 46 ›› Issue (4): 715-727.doi: 10.12122/j.issn.1673-4254.2026.04.01

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miR-24-3p靶向GSK-3β抑制铁死亡促进大鼠脊髓损伤修复

魏栋敏¹(), 王冰冰¹(), 高建忠², 翟天宇¹, 白心悦¹, 朱晶惠¹, 张灿¹, 施彩珍¹, 郝琴¹, 陈晨², 赵琳¹()

^1.延安大学延安医学院，陕西延安 716000
^2.榆林市第一医院，陕西榆林 719000

收稿日期:2025-03-27 接受日期:2025-12-09 出版日期:2026-04-20 发布日期:2026-04-24
通讯作者: 赵琳 E-mail:weidongmin274912@163.com;wbb1681628@163.com;jkpzhaolin@163.com
作者简介:魏栋敏，在读硕士研究生，E-mail: weidongmin274912@163.com
王冰冰，在读硕士研究生，E-mail: wbb1681628@163.com
第一联系人：魏栋敏、王冰冰共同为第一作者

miR-24-3p promotes spinal cord injury repair in rats by inhibiting ferroptosis via targeting GSK-3β

Dongmin WEI¹(), Bingbing WANG¹(), Jianzhong GAO², Tianyu ZHAI¹, Xinyue BAI¹, Jinghui ZHU¹, Can ZHANG¹, Caizhen SHI¹, Qin HAO¹, Chen CHEN², Lin ZHAO¹()

^1.Yan'an Medical College, Yan'an University, Yan'an 716000, China
^2.Yulin First People's Hospital, Yulin 719000, China

Received:2025-03-27 Accepted:2025-12-09 Online:2026-04-20 Published:2026-04-24
Contact: Lin ZHAO E-mail:weidongmin274912@163.com;wbb1681628@163.com;jkpzhaolin@163.com
About author:First author contact:WEI Dongmin and WANG Bingbing contributed equally to this work.
Supported by:
National Natural Science Foundation of China(81641048);国家自然科学基金(81641048);Shaanxi Social Development of Science and Technology Project(2021SF-082);陕西省科技厅项目(2021SF-082);Shaanxi Social Development of Science and Technology Project(2025SF-YBXM-014);Research Project of Yan'an University(2023JBZR-011);延安大学科技项目(2023JBZR-011)

摘要/Abstract

摘要：

目的探讨miR-24-3p促进大鼠脊髓损伤（SCI）修复的分子机制。方法构建SD大鼠SCI模型，通过qRT-PCR检测SCI后miR-24-3p的表达变化。采用立体定位仪，通过尖端固定有毛细玻璃管的微量注射器于SCI头、尾各3 mm处注射miR-24-3p agomir或阴性对照agomir。使用BBB评分评估SCI大鼠运动功能恢复情况，HE染色观察脊髓组织形态学改变，试剂盒检测SCI区域Fe²⁺含量，普鲁士蓝+DAB染色检测SCI区域铁沉积变化。采用Western blotting和免疫荧光染色检测SCI区域组织GSK-3β及铁死亡相关蛋白xCT、GPX4的表达水平。双荧光素酶报告实验验证miR-24-3p与GSK-3β的靶向关系。体外构建Erastin诱导的PC12细胞铁死亡模型，检测MDA含量变化， Western blotting和免疫荧光染色检测细胞内GSK-3β、xCT和GPX4的蛋白表达水平变化。结果在SD大鼠SCI模型中，SCI区域miR-24-3p、xCT和GPX4蛋白表达在损伤后显著降低（P<0.05）。给予miR-24-3p agomir干预后，SCI大鼠后肢运动功能明显恢复，脊髓组织病理形态得到改善，Fe²⁺含量及铁沉积减少，GSK-3β蛋白表达降低，xCT和GPX4蛋白表达增加（P<0.05）。双荧光素酶报告实验证实miR-24-3p与GSK-3β之间存在靶向关系并抑制GSK-3β的表达。PC12细胞铁死亡模型中，转染miR-24-3p mimics可显著降低细胞内MDA含量和GSK-3β蛋白表达水平，并升高xCT和GPX4的蛋白表达水平；联合转染GSK-3β抑制剂后，上述效应进一步增强。结论 miR-24-3p通过抑制GSK-3β抑制铁死亡，从而促进大鼠SCI的修复。

关键词: 脊髓损伤, miR-24-3p, GSK-3β, 铁死亡

Abstract:

Objective To investigate the molecular mechanism by which miR-24-3p promotes spinal cord injury (SCI) repair in rats. Methods The changes in spinal cord miR-24-3p expression was detected in a SD rat model of SCI with qRT-PCR. Using a stereotaxic apparatus, miR-24-3p agomir or a negative control reagent was microinjected at 3 mm rostral and caudal to the SCI epicenter of the rats. Motor function recovery of the SCI rats was evaluated with BBB scores, histopathological changes and Fe²⁺ content in the SCI area were examined with HE staining and a commercial assay kit, and the changes in iron deposition in the SCI area was observed using Prussian blue staining with DAB. Western blotting and immunofluorescence staining were used to detect expressions of glycogen synthase kinase-3β (GSK-3β) and ferroptosis-related proteins xCT and GPX4 in the injured tissue. The targeted regulatory relationship between miR-24-3p and GSK-3β was verified using dual-luciferase reporter assay. In PC12 cells with erastin-induced ferroptosis, malondialdehyde (MDA) content was detected and the expression levels of GSK-3β, xCT and GPX4 proteins were determined by Western blotting and immunofluorescence staining. Results The expression of miR-24-3p and protein levels of xCT and GPX4 were significantly decreased in the SCI area of the rat models. Treatment with miR-24-3p agomir significantly improved hindlimb motor function of the SCI rats, alleviated spinal cord pathologies, reduced Fe²⁺ content, iron deposition and GSK-3β protein expression, and upregulated xCT and GPX4 protein expressions in the SCI area. Dual-luciferase reporter assay confirmed targeted inhibition of GSK-3β by miR-24-3p. In erastin-induced PC12 cells, transfection with miR-24-3p mimics significantly decreased intracellular MDA content and GSK-3β protein expression and increased xCT and GPX4 protein levels, and these effects were enhanced by co-transfection with GSK-3β inhibitor. Conclusion miR-24-3p promotes repair of SCI in rats by inhibiting ferroptosis via targeted suppression of GSK-3β.

Key words: spinal cord injury, miR-24-3p, glycogen synthase kinase-3β, ferroptosis

魏栋敏, 王冰冰, 高建忠, 翟天宇, 白心悦, 朱晶惠, 张灿, 施彩珍, 郝琴, 陈晨, 赵琳. miR-24-3p靶向GSK-3β抑制铁死亡促进大鼠脊髓损伤修复[J]. 南方医科大学学报, 2026, 46(4): 715-727.

Dongmin WEI, Bingbing WANG, Jianzhong GAO, Tianyu ZHAI, Xinyue BAI, Jinghui ZHU, Can ZHANG, Caizhen SHI, Qin HAO, Chen CHEN, Lin ZHAO. miR-24-3p promotes spinal cord injury repair in rats by inhibiting ferroptosis via targeting GSK-3β[J]. Journal of Southern Medical University, 2026, 46(4): 715-727.

图/表 6

Fig.1 Injection of miR-24-3p promotes recovery of spinal cord morphology and motor function in rats after SCI. A: qRT-PCR detection of miR-24-3p expression in rat spinal cord tissue (Mean±SD, n=3; ***P<0.01). B: Western blotting for detecting expression levels of xCT and GPX4 proteins in rat spinal cord tissue (Mean±SD, n=3; **P<0.01). C: HE staining of rat spinal cord tissues in different groups (Original magnification: ×10; scale bar=100 μm). D: BBB scores of the rats in different groups at different time points (Mean±SD, n=6; ***P<0.001 vs SCI group; ###P<0.001 vs SCI+NC group).

Fig.2 miR-24-3p treatment alleviates ferroptosis in the spinal cord tissues of SCI rats. A: Analysis of Fe2+ accumulation in the spinal cord of the rats 3 days after SCI (***P<0.001, ###P<0.001). B: Prussian blue and DAB staining of spinal cord tissues of the rats in different groups (×10). C: Relative expression levels of xCT and GPX4 proteins in rat spinal cord tissues detected by Western blotting (*P<0.05, **P<0.01, #P<0.05, ##P<0.01). D: Immunofluorescence staining for xCT and GPX4 in the spinal cord of the rats in different groups (×10; #P<0.05, ***P<0.001). All data are presented as Mean±SD (n=3).

Fig.3 Targeting relationship between miR-24-3p and GSK-3β. A: Relative expression levels of GSK-3β proteins in rat spinal cord tissue detected by Western blotting (Mean±SD, n=3; **P<0.01, #P<0.05). B: Schematic diagram of the binding site between rno-miR-24-3p and r-GSK-3β-3UTR. C: Dual-luciferase reporter gene assay for detecting the interaction between rno-miR-24-3p and r-GSK-3β-3UTR (Mean±SD, n=3; ***P<0.001).

Fig.4 Effect of transfection with miR-24-3p mimics on erastin-induced ferroptosis in PC12 cells. A: CCK-8 assay for assessing the effect of different concentrations of erastin on PC12 cell viability (*P<0.05, **P<0.01, ***P<0.001). B: Fluorescence staining for evaluating transfection efficiency of miR-24-3p mimics in PC12 cells (×20). C: MDA assay results (***P<0.001, ###P<0.001). D: Expression levels of GSK-3β, xCT, and GPX4 proteins in PC12 cells detected by Western blotting (***P<0.001, ##P<0.01, ###P<0.001). E: Immunofluorescence staining for detecting GSK-3β, xCT, and GPX4 expressions in PC12 cells with different treatments (×20; **P<0.01, ***P<0.001, ##P<0.01, ###P<0.001). Data are presented as Mean±SD (n=3).

Fig.5 Effect of GSK-3β inhibitor on expression of ferroptosis-related proteins in erastin-treated PC12 cells. A: Expression levels of GSK-3β, xCT, and GPX4 proteins in erasting-treated PC12 cells transfected with miR-24-3p mimics and GSK-3β inhibitor (*P<0.05, **P<0.01). B: Immunofluorescence staining for GSK-3β, xCT, and GPX4 in erasting-treated PC12 cells transfected with miR-24-3p mimics and GSK-3β inhibitor (×20; **P<0.01, ***P<0.001). Data are presented as Mean±SD (n=3).

Fig.6 Schematic diagram of miR-24-3p targeting GSK-3β to regulate the xCT/GPX4 axis and inhibit ferroptosis in spinal cord injury.

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miR-24-3p靶向GSK-3β抑制铁死亡促进大鼠脊髓损伤修复

miR-24-3p promotes spinal cord injury repair in rats by inhibiting ferroptosis via targeting GSK-3β

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