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Updated: Feb 13, 2026
Measuring Post-Stroke Cerebral Edema, Infarct Zone and Blood-Brain Barrier Breakdown in a Single Set of Rodent Brain Samples
Published on: October 23, 2020
Experimental Study on Changes in the Structure of the Blood-Brain Barrier after Treatment with Bevacizumab for
Xiao-Yi Lin1, Muhammad Usman2, Li Ai3
1Department of Radiology, Chenjiaqiao Hospital of Shapingba District, Chongqing, 401331, People's Republic of China.
Objective:
To investigate the effect of bevacizumab on traumatic cerebral edema and its relationship with the blood-brain barrier (BBB) in traumatic brain injury (TBI).
Methods:
Seventy rats were randomly divided into the control, sham, TBI, TBI + normal saline (TBI-NS), and TBI + bevacizumab (TBI-Beva) groups. A total of 24 h after TBI, western blotting was used to detect vascular endothelial growth factor (VEGF) and occludin. Pathological examination was used to observe cerebral edema. Magnetic resonance imaging (MRI) was performed to observe cerebral edema and brain tissue enhancement. Transmission electron microscope was used to observe the structure of BBB. Immunofluorescence was used to detect immunoglobulin G (IgG) intensity.
Results:
The expression of VEGF increased after TBI, whereas bevacizumab inhibited the expression of VEGF. MRI showed obvious cerebral edema and enhancement areas around the trauma site after TBI, and bevacizumab treatment reduced both the cerebral edema and enhancement range. Compared with the Sham group, cerebral edema occurred after TBI, including vasogenic and intracellular edema, but bevacizumab treatment simultaneously reduced both types of cerebral edema. The expression of occludin was down-regulated and IgG intensity was up-regulated, and the BBB structure was damaged after TBI. The expression of occludin was up-regulated and IgG intensity was down-regulated after treatment with bevacizumab. Meanwhile, the extent of damage to the BBB structure was reduced.
Conclusion:
Bevacizumab promotes recovery from traumatic cerebral edema by repairing BBB damage and is a potential drug for TBI treatment.
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