Özevren H, Deveci E, Tuncer M C
Department of Anatomy, Faculty of Medicine, University of Dicle, 21280 Diyarbakır, Turkey.
Folia Morphol (Warsz). 2018;77(4):642-648. doi: 10.5603/FM.a2018.0029. Epub 2018 Mar 23.
Traumatic brain injury (TBI) is in part associated with the disruption of the blood-brain barrier. In this study, we analysed the histopathological changes in E-cadherin and vascular endothelial growth factor (VEGF) expression after TBI in rats.
The rats were divided into two groups as the control and the trauma groups. Sprague-Dawley rats were subjected to TBI with a weight-drop device using 300 g/1 m weight-height impact. After 5 days of TBI, blood samples were taken under ketamine hydroxide anaesthesia and biochemical analyses were performed. The control and trauma groups were compared in terms of biochemical values.
There was no change in glutathione (GSH) levels and blood-brain barier permeability. However, malondialdehyde (MDA) and myeloperoxidase (MPO) activity levels increased in the trauma group. In the histopathological examination, choroid plexus in the lateral ventricle, near the pia mater membrane, was removed. In the traumatic group, some of epithelial cells were hyperplasic. Some of them were peeled off the apical surface and had local degeneration.
In addition, we observed congestion in capillary vessels and mononuclear cell infiltration around the vessels. After TBI, the increase in VEGF levels, vascular permeability, and interaction with VEGF receptors in endothelial cells lead to oedema of the vessel wall. On the other hand, E-cadherin expression decreased in the tight-junction structures between epithelial cells and basal membrane, resulting in an increase in cerebrospinal fluid in the intervillous area.
创伤性脑损伤（TBI）部分与血脑屏障的破坏有关。在本研究中，我们分析了大鼠TBI后E-钙黏蛋白和血管内皮生长因子（VEGF）表达的组织病理学变化。
将大鼠分为对照组和创伤组。使用300 g/1 m重量-高度冲击的重物下落装置对Sprague-Dawley大鼠进行TBI。TBI 5天后，在氢氧化氯胺酮麻醉下采集血样并进行生化分析。比较对照组和创伤组的生化值。
谷胱甘肽（GSH）水平和血脑屏障通透性无变化。然而，创伤组丙二醛（MDA）和髓过氧化物酶（MPO）活性水平升高。在组织病理学检查中，切除软脑膜附近侧脑室的脉络丛。在创伤组中，一些上皮细胞增生。其中一些从顶端表面脱落并出现局部变性。
此外，我们观察到毛细血管充血和血管周围单核细胞浸润。TBI后，VEGF水平升高、血管通透性增加以及内皮细胞中VEGF受体的相互作用导致血管壁水肿。另一方面，上皮细胞与基底膜之间紧密连接结构中的E-钙黏蛋白表达降低，导致绒毛间隙脑脊液增加。
