Background Although some studies have reported that aquaporin-4 （AQP4） plays an important role in the brain edema after traumatic brain injury （TBI）, little is known about the AQP4 expression in the early stage of TBI, or about the correlation between the structural damage to the blood-brain barrier （BBB） and angioedema. The aim of this project was to investigate the relationship between AQP4 expression and damage to the BBB at early stages of TBI. Methods One hundred and twenty healthy adult Wistar rats were randomly divided into two groups： sham operation group （SO） and TBI group. The TBI group was divided into five sub-groups according to the different time intervals： 1, 3, 6, 12, and 24 hours. The brains of the animals were taken out at different time points after TBI to measure brain water content. The cerebral edema and BBB changes in structure were examined with an optical microscopy （OM） and transmission electron microscopy （TEM）, and the IgG content and AQP4 protein expression in traumatic brain tissue were determined by means of immunohistochemistry and Western blotting. The data were analyzed with SPSS 13.0 statistical software. Results In the SO group, tissue was negative for IgG, and there were no abnormalities in brain water content or AQP4 expression. In the TBI group, brain water content significantly increased at 6 hours and peaked at 24 hours following injury. IgG expression significantly increased from 1 to 6 hours following injury, and remained at a high level at 24 hours. Pathological observation revealed BBB damage at 1 hour following injury. Angioedema appeared at 1 hour, was gradually aggravated, and became obvious at 6 hours. Intracellular edema occurred at 3 hours, with the presence of large glial cell bodies and mitochondrial swelling. These phenomena were aggravated with time and became obvious at 12 hours. In addition, microglial proliferation was visible at 24 hours. AQP4 protein expression were reduced at 1 hour, lowest at 6 hours, and began to increase a
Objective:To establish stable and controllable brain injury with accurate degree and good repeatability in rat model.Methods:Controlled cortical impact(CCI) device was used to prepare for the rat brain injury model by the impact head of different model(Group A No.4.Group B No.5,Group C No.6) and the impact depth(Group A:1.5-2.0 mm.Group B:2.5-3.0 mm.Group C:3.5-4.0mm) with impact time of 0.1 s and impact velocity of 2.5 m/s.Twelve rats with three months of age were used in each group(the impact depth of every two rats was added 1 mm respectively).After modeling for 1 h,magnetic resonance imaging(MRI) was received and brain histopathology was observed to assess degree of injury by model parameter's of three groups.Results:After modeling of Group A,MRI showed that the cortex structure was damaged with a small amount of bleeding in center and mild edema around,and the total volume of injury was(28.69±4.94)mm^3.Pathology revealed the injury was confined to the superficial cortical with mild edema of nerve cell,which was assessed as mild cerebral contusion.While after modeling,MRI of Group B showed that the structure of cortex and medulla were damaged simultaneously and extended to cerebral nuclei zone,With 4 cases of hematoma in the center and larger edema range around,and the total volume of injury was(78.38±9.28) mm^3.Pathology revealed the injury range was reached nuclei zone,with swell of nerve cell and mitochondria,which was assessed to moderate cerebral contusion.After modeling of Group C,MRI showed that extensive tissue injury was appeared in cortex and medulla and deep nuclei,with 9 cases of hematoma and large edema signal of surrounding tissue T2W1,while in 5 cases,lateral nucleus of injury signal was increased,and the total volume of injury was(135.89±24.80)mm^3.Pathology revealed the deep cerebral nuclei was damaged,with the disappearance of neuronal structure and vacuolization of mitochondria,which was assessed as severe cerebral contusion.MRI changes were consistent with pathological changes in three
