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慢性压迫性脊髓损伤大鼠模型中神经血管单元的超微结构特征

Ultrastructural Features of Neurovascular Units in a Rat Model of Chronic Compressive Spinal Cord Injury.

作者信息

Xu Jinghui, Long Houqing, Chen Wenli, Cheng Xing, Yu Haoyang, Huang Yangliang, Wang Xiaobo, Li Fobao

机构信息

Department of Spine Surgery, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.

Guangdong Provincial Key Laboratory of Orthopedics and Traumatology, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.

出版信息

Front Neuroanat. 2018 Jan 10;11:136. doi: 10.3389/fnana.2017.00136. eCollection 2017.

DOI:10.3389/fnana.2017.00136
PMID:29375327
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5767600/
Abstract

Chronic spinal cord compression is the most common cause of spinal cord impairment worldwide. Objective of this study is to assess the ultrastructural features of the neurovascular unit (NVU) in a rat model of chronic compressive spinal cord injury, 24 rats were divided into two groups: the control group ( = 12), and the compression group ( = 12). A C6 semi-laminectomy was performed in the control group, whereas a water-absorbent polyurethane polymer was implanted into the C6 epidural space in the compression group. The Basso Beattie Bresnahan (BBB) scores and the somatosensory evoked potentials (SEP) were used to evaluate neurological functions. Transmission Electron Microscopy (TEM) was performed to investigate the change of NVU at the 28th day after modeling. Compared with the control group, the compression group shows a significant reduction ( < 0.05) of BBB score and a significant severity ( < 0.05) of abnormal SEP. TEM results of the compression group showed a striking increase in endothelial caveolae and vacuoles; a number of small spaces in tight junctions; a significant increase in pericyte processing area and vessel coverage; an expansion of the basement membrane region; swollen astrocyte endfeet and mitochondria; and the degeneration of neurons and axons. Our study revealed that damage to NVU components occurred followed by chronic compressive spinal cord injury. Several compensatory changes characterized by thicker endothelium, expansive BM, increased pericyte processing area and vessel coverage were also observed.

摘要

慢性脊髓压迫是全球范围内脊髓损伤最常见的原因。本研究的目的是评估慢性压迫性脊髓损伤大鼠模型中神经血管单元(NVU)的超微结构特征,将24只大鼠分为两组:对照组(n = 12)和压迫组(n = 12)。对照组行C6半椎板切除术,而压迫组将吸水性聚氨酯聚合物植入C6硬膜外间隙。采用Basso Beattie Bresnahan(BBB)评分和体感诱发电位(SEP)评估神经功能。在建模后第28天进行透射电子显微镜(TEM)检查以研究NVU的变化。与对照组相比,压迫组BBB评分显著降低(P < 0.05),SEP异常程度显著加重(P < 0.05)。压迫组的TEM结果显示内皮小窝和空泡显著增加;紧密连接中有许多小间隙;周细胞加工区域和血管覆盖率显著增加;基底膜区域扩大;星形胶质细胞终足和线粒体肿胀;神经元和轴突退变。我们的研究表明,慢性压迫性脊髓损伤后会发生NVU成分的损伤。还观察到一些以更厚的内皮、扩张的基底膜、增加的周细胞加工区域和血管覆盖率为特征的代偿性变化。

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Histological, immunohistochemical and ultrastructural study of secondary compressed spinal cord injury in a rat model.大鼠模型中继发性压迫性脊髓损伤的组织学、免疫组织化学及超微结构研究
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Ultrastructural analysis of blood-brain barrier breakdown in the peri-infarct zone in young adult and aged mice.
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The ferroptosis activity is associated with neurological recovery following chronic compressive spinal cord injury.铁死亡活性与慢性压迫性脊髓损伤后的神经功能恢复有关。
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