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BACKGROUND: Preliminary findings have shown that radiation can impair the mouse blood-brain barrier, which is a cause of secondary brain injury. However, there is little information concerning radiation effects on fibrinogen in plasma and fibrinogen deposition in brain tissue. OBJECTIVE: To establish the mouse model of radiation-induced brain injury, to observe the changes of fibrinogen in plasma and brain tissue, and to further understand the mechanism of radiation-induced brain injury. METHODS: Fifty Kunming mice were randomly divided into irradiation and control groups (n=25 per group). Irradiation group rats were irradiated by 60Co γ, 10 Gy, once every other day, and the total dose was 30 Gy. Learning and memory abilities were tested by Morris Water Maze before and after irradiation, the content of fibrinogen in plasma was detected, then fibrinogen in CA3 region of the hippocampus was determined by immunohistochemistry, and the ultrastructural changes of the blood-brain barrier were investigated under transmission electron microscope . RESULTS AND CONCLUSION: Compared with the control group, the swimming time and distance of the irradiated mice were reduced in the target quadrant (P < 0.05), while fibrinogen was increased in plasma (P < 0.001) and deposited in hippocampal CA3 region. The translucent zone around the basement membrane of blood-brain barrier in the irradiation group was observed under electron microscope. These results suggest that irradiation can increase fibrinogen in plasma and brain, and the fibrinogen deposited in the brain may be the cause of secondary brain injury. [ABSTRACT FROM AUTHOR]

BACKGROUND: Radiotherapy is one of the main methods for the treatment of brain tumors, which significantly improves the clinical efficacy. However, its side effects on normal brain tissue seriously affect the quality of life of patients. Therefore, it is particularly important to find a way to effectively prevent the damage of normal brain tissue and to study its mechanism. OBJECTIVE: To explore the effect and mechanism of Laminaria japonica polysaccharide intervention on radiation-induced brain injury in mice. METHODS: Ninety-six male Kunming mice, SPF grade, were randomly divided into four groups (n=24 per group): a control group, an irradiation group, a Laminaria japonica polysaccharide (LJP) group, and an irradiation+LJP group. All mice were given 7-day continuous administration before radiation, and then 60Go γ-rays (30 Gy) were used to establish a radiation brain injury model in mice. Immunofluorescence method was used to detect the expression of fibrinogen and activation and deposition of astrocytes in the brain tissue. The ultrastructural changes of the cerebrovascular system were investigated under transmission electron microscope. The motion trails of the mice in the Morris water maze were observed before and after treatment. RESULTS AND CONCLUSION: After radiotherapy, the expression of fibrinogen in brain tissue was significantly increased, and astrocytes were obviously activated, while the radiation plus LJP intervention significantly relieved the deposition of fibrinogen in mice. Under the electron microscope, the brain vascular endothelial cells swelled, the basement membrane was broken and shed, and the blood-brain barrier structure changed after radiation. However, the ultrastructural morphology of the mouse blood-brain barrier in the radiation+LJP group was similar to that of the control group. After radiation, the number of times and activity time of the mice passing through the platform area was significantly reduced in the Morris water maze test (P < 0.05), while the activities of the radiation mice in the platform area showed an increasing trend after the LJP intervention. These results suggest that the protective effect of LJP on radiation-induced brain injury may be mainly achieved by maintaining the stability of the blood-brain barrier structure and regulating its permeability. [ABSTRACT FROM AUTHOR]