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

Traumatic brain injury (TBI) is in part associated with the disruption of the blood-brain barrier. In this study, we analyzed the histopathological changes in E-cadherin and VEGF expression after traumatic brain injury in rats. The rats were divided into 2 groups as the control and the trauma groups. Sprague-Dawley rats were subjected to traumatic brain injury with a weight-drop device using 300 g⁻¹ m weight-height impact. After 5 days of traumatic brain injury, blood samples were taken under ketamine hydroxide anesthesia and biochemical analyzes 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 barrier permeability. However, malondialdehyde (MDA) and myeloperoxidase activity (MPO) levels increased in the trauma group. In the histopathological examination, choroid plexus in the lateral ventricule, near the piamater membrane, was removed. In the traumatic group, some of epithelial cells were hyperplasic, some of were with local degeneration with peeled off from apical surface. In addition, we observed that congestion in capillary vessels and mononuclear cell infiltration around the vessels. After traumatic brain injury, the increase in vascular endothelial growth factor (VEGF) levels, vascular permeability, and interaction with VEGF receptors in endothelial cells lead to edema in 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.