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

机译:慢性压迫性脊髓损伤大鼠模型中神经血管单位的超微结构特征

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摘要

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 SD rats were divided into two groups: the control group (n = 12), and the compression group (n = 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 (P < 0.05) of BBB score and a significant severity (P < 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.
机译:慢性脊髓压迫是全世界脊髓损伤的最常见原因。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位(NVU)的超微结构特征,将24只SD大鼠分为两组:对照组(n = 12)和压迫组(n = 12)。对照组进行了C6半椎板切除术,而压缩组在C6硬膜外腔植入了吸水性聚氨酯聚合物。 Basso Beattie Bresnahan(BBB)评分和体感诱发电位(SEP)用于评估神经功能。建模后第28天,进行了透射电子显微镜(TEM)研究NVU的变化。与对照组相比,压迫组的BBB评分显着降低(P <0.05),SEP异常的严重程度也显着(P <0.05)。压迫组的TEM结果显示内皮小窝和液泡显着增加。紧密连接处有许多小空间;周细胞处理面积和容器覆盖率显着增加;基底膜区域的扩展;星形胶质细胞末端和线粒体肿胀;以及神经元和轴突的变性。我们的研究表明,对NVU组件的损害是由慢性压缩性脊髓损伤引起的。还观察到了一些补偿性变化,其特征是内皮增厚,BM膨胀,周细胞加工面积增加和血管覆盖。

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