Histopathological changes in the choroid plexus after traumatic brain injury in the rats: a histologic and immunohistochemical study.

BACKGROUND: 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.
MATERIALS AND METHODS: 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.
RESULTS: 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.
CONCLUSIONS: 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.