放射性脑损伤模型小鼠纤维蛋白原的变化

Changes of fibrinogen in a mouse model of radiation-induced brain injury

背景:前期研究发现放射破坏小鼠血脑屏障,而放射致损伤的血脑屏障是继发性脑损伤的原因,但目前有关放射因素对血浆纤维蛋白原及脑组织中纤维蛋白原沉积的影响报道甚少。目的:建立放射性脑损伤模型,观察放射后血浆中纤维蛋白原的变化及其在脑组织中沉积的情况,探讨放射性脑损伤机制。方法:50只昆明小鼠随机分为放射组、对照组,每组各25只,放射组予^(60)Coγ射线照射,15 Gy/次,隔天照射,共30 Gy。放射前、后分别采用Morris水迷宫观察小鼠学习记忆能力的变化,神经行为结束后,检测血浆中纤维蛋白原的含量,采用免疫组织化学方法观察海马CA3区纤维蛋白原的表达,并在电镜下观察其血脑屏障结构变化。结果与结论:(1)与对照组相比,放射组小鼠放射后在目标区域停留的时间和路程明显减少(P<0.05);(2)血浆纤维蛋白原显著升高(P<0.001),海马CA3区有大量纤维蛋白原沉积,电镜下血脑屏障基膜周围出现透亮区;(3)结果说明,放射可致血浆中纤维蛋白原升高,沉积于脑组织的纤维蛋白原可能是继发性脑损伤的原因。

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 60Coγ,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.