中国神经再生研究(英文版) ›› 2026, Vol. 21 ›› Issue (6): 2475-2484.doi: 10.4103/NRR.NRR-D-24-01098

• 原著:脊髓损伤修复保护与再生 • 上一篇    下一篇

光生物调节修复脊髓损伤小鼠血脊髓屏障

  

  • 出版日期:2026-06-15 发布日期:2026-04-18
  • 基金资助:
    国家自然科学基金项目(82471411),陕西省重点研发计划项目(2023-ZDLSF-12)

Photobiomodulation repairs the blood–spinal cord barrier in a mouse model of spinal cord injury

Yangguang Ma1, #, Yi Liu2, #, Dongsheng Pan1, Jiawei Zhang1, Zhuowen Liang1, Yi Wang2, Xueyu Hu1, Zhe Wang1, *, Tan Ding1, *   

  1. 1Department of Orthopedics, Xijing Hospital, Fourth Military Medical University, Xi’an, Shaanxi Province, China; 
    2Shaanxi Shuoguang Qifu Medical Technology Co., Ltd., Xianyang, Shaanxi Province, China

  • Online:2026-06-15 Published:2026-04-18
  • Supported by:
    This study was supported by the National Natural Science Foundation of China, No. 82471411 (to ZW and TD); and the Key Research and Development Program of Shaanxi Province, No. 2023-ZDLSF-12 (to TD).

摘要:

血脊髓屏障对于维持中枢神经系统稳态至关重要。脊髓损伤后,内皮细胞内自噬通量异常,继而损害血脊髓屏障的完整性。后者进一步加剧免疫炎症细胞的广泛浸润,导致神经炎症反应加剧、神经元死亡和神经元再生障碍。既往有研究显示,光生物调节可通过抑制炎性细胞向损伤部位的募集和恢复神经元线粒体功能,促进脊髓损伤后受损神经的再生。然而,其作用机制尚不明确。为此,实验构建了脊髓挤压损伤小鼠模型,并以光生物调节进行干预。结果显示,光生物调节有助于清除脊髓损伤小鼠血管内皮细胞中受损的线粒体,促进后肢运动功能的恢复。进而对微血管内皮细胞的氧糖剥夺bEnd.3细胞模型行光生物调节,发现光生物调节的作用是通过激活PINK1/Parkin通路介导的,且光生物调节可降低线粒体氧化应激水平,并增强血脊髓屏障内紧密连接蛋白的表达。由此提示,光生物调节可通过PINK1/Parkin通路激活内皮细胞线粒体自噬,进而促进脊髓损伤血脊髓屏障的修复。


https://orcid.org/0000-0002-7573-1583 (Zhe Wang); https://orcid.org/0000-0001-6243-0004 (Tan Ding)

关键词: 脊髓损伤, 血脊髓屏障, 光生物调节, 内皮细胞, 线粒体, 自噬, 修复, 神经炎症, 紧密结合, PTEN诱导激酶1

Abstract: The blood–spinal cord barrier is crucial for preserving homeostasis of the central nervous system. After spinal cord injury, autophagic flux within endothelial cells is disrupted, compromising the integrity of the blood–spinal cord barrier. This disruption facilitates extensive infiltration of inflammatory cells, resulting in exacerbated neuroinflammatory responses, neuronal death, and impaired neuronal regeneration. Previous research has demonstrated that photobiomodulation promotes the regeneration of damaged nerves following spinal cord injury by inhibiting the recruitment of inflammatory cells to the injured site and restoring neuronal mitochondrial function. However, the precise mechanisms by which photobiomodulation regulates neuroinflammation remain incompletely elucidated. In this study, we established a mouse model of spinal cord injury and assessed the effects of photobiomodulation treatment. Photobiomodulation effectively cleared damaged mitochondria from endothelial cells in mice, promoting recovery of hindlimb motor function. Using microvascular endothelial bEnd.3 cells subjected to oxygen–glucose deprivation, we found that the effects of photobiomodulation were mediated through activation of the PINK1/ Parkin pathway. Additionally, photobiomodulation reduced mitochondrial oxidative stress levels and increased the expression of tight junction proteins within the blood–spinal cord barrier. Our findings suggest that photobiomodulation activates mitochondrial autophagy in endothelial cells through the PINK1/Parkin pathway, thereby promoting repair of the blood–spinal cord barrier following spinal cord injury. 

Key words: autophagy, blood–spinal cord barrier, endothelial cell, mitochondria, neuroinflammatory, photobiomodulation, PTEN-induced kinase 1, repair, spinal cord injury, tight junction