In the in vivo experiment， the TBI models of adult C57BL/6 mice were prepared by hydraulic craniocerebral percussion instrument， and the experimental mice were randomly divided into sham operation group and TBI group. The brain tissue was collected 24 h after TBI for the detection of water content in brain tissue； Evans blue（EB） injection was used to detect the blood brain barrier permeability（EB level） and HE staining was used to observe the pathomorphology of brain tissue of the mice. Immunofluorescence staining method was performed to detect the expression levels of vascular endothelial growth factor receptor 1（VEGFR1） and platelet-endothelial cell adhesion molecule CD31 proteins in brain tissue of the mice. In the in vitro experiment， the C57BL16 mice with CD47 knockout and endogenous expression of green fluorescent protein（GFP） labeled （CD47KO-GFP group） and wild type （WT） mice （WT group） were selected.The TBI models were prepared with hydraulic craniocerebral percussion.The brain microvascular endothelial cells were extracted and mixedly cultured. The regeneration and tube-forming capacities of cerebral microvascular endothelial cells after TBI were observed by fluorescence microscope； immunofluorescence staining method was used to detect the activation of nuclear factor-κB（NF-κB） in the cerebral microvascular endothelial cells in injured area of the mice.

Compared with sham operation group， the water content in brain tissue and EB level of the mice in TBI group were significantly increased （P<0.05）. The HE staining results showed that compared with sham operation group， the brain tissue structure of the mice in TBI group was unrecognizable and the bleeding spots were obvious. The immunofluorescence staining results showed that compared with sham operation group， the expression levels of VEGFR1 and CD31 proteins in brain tissue of the mice in TBI group were significantly increased（P<0.01）. The fluorescence microscope results showed that compared with WT group，the number of brain microvascular endothelial cells participating in angiogensis of the mice in CD47KO-GFP group was significantly increased（P<0.05）. The immunofluorescence staining results showed that compared with WT group，the activation of NF-κB in the cerebral microvascular endothelial cells in CD47KO-GFP group was decreased significantly.

After TBI， the blood brain barrier permeability and angiogenesis of injured brain tissue are increased significantly， and CD47 knockout can promote the angiogenesis.