中国组织工程研究

中国组织工程研究 ›› 2026, Vol. 30 ›› Issue (24): 6196-6206.doi: 10.12307/2026.293

• 脊柱组织构建 spinal tissue construction • 上一篇    下一篇

急性和短期运动干预脊髓损伤亚急性期大鼠腓肠肌的分子动态特征

魏心怡1，郑  艳2，陈  前3，任佳佳1，李  健4   

  1. 1华东师范大学体育与健康学院，上海市   200241；2苏州大学体育学院，江苏省苏州市   215021；3西安石油大学体育学院，陕西省西安市   710065；4北京大学医学部，北京市   100191

  • 收稿日期:2025-07-19 修回日期:2025-12-18 出版日期:2026-08-28 发布日期:2026-01-29
  • 通讯作者: 李健，博士，助理研究员，北京大学医学部，北京市 100191
  • 作者简介:魏心怡，女，2001年生，山东省潍坊市人，汉族，硕士，主要从事运动神经科学领域研究。

Molecular dynamic characteristics of rat gastrocnemius muscle under acute and short-term exercise intervention during the subacute phase of spinal cord injury

Wei Xinyi1, Zheng Yan2, Chen Qian3, Ren Jiajia1, Li Jian4   

  1. 1School of Physical Education and Health, East China Normal University, Shanghai 200241, China; 2School of Physical Education, Soochow University, Suzhou 215021, Jiangsu Province, China; 3School of Physical Education, Xi’an Shiyou University, Xi’an 710065, Shaanxi Province, China; 4Peking University Health Science Center, Beijing 100191, China
  • Received:2025-07-19 Revised:2025-12-18 Online:2026-08-28 Published:2026-01-29
  • Contact: Li Jian, MD, Assistant researcher, Peking University Health Science Center, Beijing 100191, China
  • About author:Wei Xinyi, MS, School of Physical Education and Health, East China Normal University, Shanghai 200241, China

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摘要：



文题释义：
时序性影响：脊髓损伤亚急性期不同时间窗口内，运动干预诱导的下肢骨骼肌分子网络动态重编程现象，主要表现为：①差异基因表达的时序性波动：如急性干预显著富集于细胞周期调控通路，而短期干预以炎症反应负向调控为主导；②信号通路的阶段特异性激活/抑制：急性运动显著上调了细胞周期、DNA复制和运动蛋白通路，短期干预显著下调了白细胞介素17通路、肿瘤坏死因子通路，Janus激酶/信号转导和转录活化因子通路与丝裂原活化蛋白激酶通路，这揭示了干预时机与分子应答存在严格的时间-效应耦合规律。
下肢肌肉分子表达：脊髓损伤后下肢肌肉的分子表达重构，本质上是运动干预调控神经-肌肉修复微环境的表观遗传学应答。①GSEA富集通路显示：急性运动干预诱导腓肠肌差异表达基因显著富集于细胞周期进程；而短期干预组差异表达基因则与炎症反应密切相关；②蛋白互作网络拓扑特征：基于STRING数据库构建的蛋白互作网络显示，急性运动干预核心模块以Shh、Top2a为枢纽节点，而短期干预中心模块以Comp、Grik2等为关键调控因子。

背景：脊髓损伤引发神经-肌肉系统级联损伤涉及到中枢模式发生器功能失活及外周肌肉分子网络紊乱，运动能够调控特征基因并促进脊髓损伤康复。
目的：利用生物信息学筛选靶向运动调控的特征基因，探索运动干预调节脊髓损伤恢复的发生机制。
方法：通过GEO数据库下载基于GPL1355平台的GSE45550数据集，筛选大鼠脊髓损伤亚急性期急性运动与短期运动干预所调控的相关差异基因，并对相关差异基因进行GO功能富集分析、KEGG信号通路、GSEA富集分析，以及建立蛋白互作网络。
结果与结论：①大鼠脊髓损伤亚急性期进行急性运动干预后腓肠肌106个基因上调，97个基因下调；短期运动干预后138个基因上调，105个基因下调；②GO分析表明，急性运动干预后差异基因主要富集于染色体分离；短期运动干预主要促进了信号转导等过程；KEGG分析表明急性运动干预主要与胃酸分泌、运动蛋白通路上调等有关；短期运动干预主要涉及神经活性配体受体互作上调及部分炎症信号通路下调；③GSEA分析显示，急性运动干预主要上调细胞周期、DNA分离；短期运动干预主要下调白细胞介素17信号、肿瘤坏死因子信号通路；④蛋白互作网络显示，急性运动干预与短期运动干预分别形成2，3个中心作用模块。总而言之，急性运动干预显著激活细胞增殖相关通路(如细胞周期、有丝分裂)，上调Top2a、Sele等促增殖基因表达；而短期干预则通过下调白细胞介素17、肿瘤坏死因子等炎症通路，下调COMP等因子表达发挥抗炎作用，这些发现为脊髓损伤康复的分子机制研究提供了参考依据。

https://orcid.org/0009-0004-9732-7129 (魏心怡) 


中国组织工程研究杂志出版内容重点：干细胞；骨髓干细胞；造血干细胞；脂肪干细胞；肿瘤干细胞；胚胎干细胞；脐带脐血干细胞；干细胞诱导；干细胞分化；组织工程

关键词: 脊髓损伤, 运动干预, 分子机制, 生物信息学, 时序性, 康复, 细胞周期, 炎症通路

Abstract: BACKGROUND: Spinal cord injury triggers a cascade of neuro-muscular system damage, involving central pattern generator dysfunction and peripheral muscle molecular network disruptions. Exercise can regulate key genes and promote the recovery of spinal cord injury.
OBJECTIVE: To identify exercise-regulated key genes through bioinformatics analysis and explore the mechanisms by which exercise intervention facilitates the recovery of spinal cord injury. 
METHODS: The GSE45550 dataset based on the GPL1355 platform was obtained from the Gene Expression Omnibus (GEO) database. Differentially expressed genes regulated by acute and short-term exercise interventions during the subacute phase of spinal cord injury in rats were identified. Gene Ontology functional enrichment analysis, Kyoto Encyclopedia of Genes and Genomes pathway analysis, and Gene Set Enrichment Analysis were performed on these differentially expressed genes, and a protein-protein interaction network was constructed.
RESULTS AND CONCLUSION: (1) After acute exercise intervention in the subacute phase of spinal cord injury, 106 genes were upregulated and 97 genes were downregulated in the gastrocnemius muscle, whereas short-term exercise intervention resulted in 138 upregulated and 105 downregulated genes. (2) Gene Ontology analysis showed that acute exercise mainly enriched genes related to chromosome segregation, while short-term exercise primarily promoted signal transduction processes. Kyoto Encyclopedia of Genes and Genomes analysis revealed that acute exercise was associated with the upregulation of pathways related to gastric acid secretion and motor protein function, whereas short-term exercise upregulated neuroactive ligand-receptor interactions and downregulated inflammatory pathways. (3) Gene Set Enrichment Analysis indicated that acute exercise intervention mainly upregulated cell cycle and DNA segregation pathways, while short-term intervention led to downregulation of the interleukin-17 and tumor necrosis factor signaling pathways. (4) The protein-protein interaction network revealed two key functional modules in acute exercise intervention and three in short-term intervention. In summary, acute exercise significantly activated cell proliferation-related pathways (e.g., cell cycle and mitosis) and upregulated pro-proliferative genes such as Top2a and Sele. In contrast, short-term intervention exerted anti-inflammatory effects by downregulating interleukin-17 and tumor necrosis factor signaling pathways and reducing the expression of inflammatory factors such as COMP. These findings provide insights into molecular mechanisms of spinal cord injury recovery.

Key words: spinal cord injury, exercise intervention, molecular mechanism, bioinformatics, temporality, rehabilitation, cell cycle, inflammatory pathway

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