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中国临床药理学与治疗学 ›› 2025, Vol. 30 ›› Issue (11): 1559-1568.doi: 10.12092/j.issn.1009-2501.2025.11.014

• 综述与讲座 • 上一篇    下一篇

阳离子失衡参与继发性脊髓损伤的机制及潜在干预药物的研究进展

周明骏1,3,桑雪2,常静雯2,刘芳2,陶羽2,范方田2   

  1. 1蚌埠医科大学临床医学院,蚌埠  230030,安徽;2蚌埠医科大学药学院,安徽省生化制药工程技术研究中心,蚌埠  230030,安徽;3南方医科大学基础医学院,广州  510515,广东

  • 收稿日期:2024-03-19 修回日期:2024-04-15 出版日期:2025-11-26 发布日期:2025-12-04
  • 通讯作者: 范方田,男,博士,教授,安徽省高端人才引育行动计划领军人才特聘教授,研究方向:细胞异常代谢相关机制及中药的干预作用。 E-mail: jim@bbmu.edu.cn
  • 作者简介:周明骏,男,硕士在读,研究方向:脊髓损伤及神经药理。 E-mail: 1229306555@qq.com
  • 基金资助:
    安徽省自然科学基金(2508085MH228);蚌埠医科大学科技成果转化孵育专项(2024byzh019);安徽省研究生教育质量工程项目(2023qygzz031);安徽省高等学校科学研究项目(2023AH051972);优秀青年教师培育项目(YQZD2025059);蚌埠医科大学龙湖英才(LH250103006);安微省高端人才引育行动计划领军人才特聘教授(范方田)

Development of the mechanism of cationic imbalance in secondary spinal cord injury and potential intervention drugs

ZHOU Mingjun1,3, SANG Xue2, CHANG Jingwen2, LIU Fang2, TAO Yu2, FAN Fangtian2   

  1. 1School of Clinical Medicine, Bengbu Medical University, Bengbu 230030, Anhui, China; 2Anhui Engineering Technology Research Center of Biochemical Pharmaceuticals, School of Pharmacy Bengbu Medical University, Bengbu 230030, Anhui, China; 3School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, Guangdong, China
  • Received:2024-03-19 Revised:2024-04-15 Online:2025-11-26 Published:2025-12-04

摘要:

脊髓损伤多是由于直接或间接外力作用于脊柱从而引起脊髓的损伤,导致脊髓相应节段控制区域出现感觉运动功能障碍。脊髓损伤依照病情发生顺序及发展机制可分为原发性脊髓损伤和继发性脊髓损伤。继发性脊髓损伤是指在脊髓初次受损后,由于病理生理过程的发展,导致脊髓损伤程度进一步加重的现象。继发性脊髓损伤包括脊髓损伤后的细胞死亡、神经元的丢失、胶质细胞增生、炎症反应、免疫微环境的改变、脊髓水肿、缺血缺氧等。这些因素相互作用,导致脊髓神经元的功能和结构发生进一步的改变,加重了脊髓损伤的程度。阳离子失衡是影响继发性脊髓损伤过程中的重要因素,中枢神经系统中常见的有钠离子、钾离子、钙离子等。这些离子的浓度变化会导致神经元的兴奋性改变,从而进一步加重脊髓损伤的程度。诸多研究发现,钙离子浓度的增加会导致神经元兴奋性增加,导致神经元的细胞死亡和神经元突触连接的损失,从而加重脊髓损伤的程度;脊髓损伤后,细胞外液中钾离子浓度会增加,导致神经元兴奋性降低,从而影响神经元的功能和结构;在继发性脊髓损伤过程中,钠离子浓度的增加会导致神经元兴奋性增加,从而加重脊髓损伤的程度。总之阳离子失衡与继发性脊髓损伤密切相关,损伤后阳离子失衡会进一步加重脊髓损伤的程度。针对阳离子失衡的治疗方法可能成为继发性脊髓损伤治疗的重要策略之一。本文总结了在继发性脊髓损伤中神经元常见阳离子的变化及影响,并介绍相关药物研究进展,以期为脊髓损伤发病机制及治疗提供进一步的理论依据。

关键词: 继发性脊髓损伤, 阳离子, 钠离子, 钾离子, 钙离子, 药物治疗

Abstract:

Spinal cord injury (SCI) is an impairment caused by direct or indirect external forces acting on the spine, resulting in a sensory-motor dysfunction in corresponding segments. Spinal cord injury can be divided into primary SCI and secondary SCI according to the occurrence sequences and progression mechanism. Secondary SCI is a phenomenon of further aggravation of the extent of SCI caused by the development of pathophysiological processes due to the initial damage of the spinal cord. Secondary SCI includes cell death after SCI, such as loss of neurons, gliosis, inflammatory response, changes in the immune microenvironment, spinal cord edema, ischemia and hypoxia, etc. These factors interact to exacerbate the SCI by causing further changes to the function and structure of the spinal cord neurons. Cationic imbalance, for example, is one of the important factors that affect the process of secondary SCI. There are some common ions in the central nervous system, such as sodium, potassium and calcium, in which concentration variation can cause changes in neuronal excitability and further aggravate the SCI level. Besides, concentration variation of some common ions in the central nervous system, such as sodium, potassium and calcium, is found to cause changes in neuronal excitability and further aggravate the SCI level. The concentration of potassium ions in the extracellular fluid increases when SCI occurs, leading to a decrease in neuronal excitability, which affects neuronal function and structure. In secondary SCI, the increased concentration of sodium ions can enhance neuronal excitability, which exacerbates SCI level. In conclusion, cationic imbalance is closely related to secondary SCI, and can further aggravate the SCI level after injury. Treatment of cation imbalance may become an important strategy in the management of secondary SCI. This paper summarizes the changes and effects of common cations in neurons in secondary SCI, and introduces the relevant drug research progress to provide further theoretical basis for the pathogenesis and treatment of SCI.

Key words: secondary spinal cord injury, cation, sodium ion, potassium ion, calcium ion, drug therapy

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