动物造模,减轻脑出血 z-bio 2022-05-18 508

　　Objective To investigate the related mechanism of hypertonic saline treatment in reducing cerebral edema in rats with cerebral hemorrhage.

　　Methods Sixty male SD rats were randomly divided into control group, model group and treatment group. After the rat brain parenchyma was injected with fetal bovine serum to make a rat model of cerebral hemorrhage, the rats in the treatment group were pumped with 10% hypertonic saline through the tail vein, 0.3 mL/h, for a total of 48 h. The mortality rate of the rats in each group was compared, the brain tissue was collected, and its appearance and pathological changes were observed with the naked eye; at the same time, the brain water content and the matrix metalloproteinase-9 (MMP-9) ) to the ratio of metallopeptidase inhibitor-1 (TIMP-1) and the difference in the expression of related tight junction proteins claudins, occludin and zonula occludens-1 (ZO-1).

　　Results The mortality and brain water content of rats in the model group were significantly higher than those in the treatment group (all P<0.05). The macroscopic observation showed that the midline of the brain of the rats in the model group was obviously shifted from the side of the lesion to the contralateral side, and there was no deviation of the midline of the brain of the rats in the treatment group. Under the microscope, the edema of the brain tissue of the rats in the treatment group was significantly reduced, and the exudation of inflammatory cells was significantly reduced. In addition, the ratio of MMP-9/TIMP-1 in the brain tissue of the rats in the treatment group was significantly lower than that in the model group, while the tight junction proteins claudin-5, occludin and ZO-1 were higher than those in the model group (all P<0.05).

　　Conclusion Hypertonic saline can reduce the ratio of MMP-9/TIMP-1, stabilize the expression of tight junction proteins claudin-5, occludin and ZO-1, maintain the structural integrity of the blood-brain barrier, and improve the severity of cerebral edema after intracerebral hemorrhage. Reduce the mortality of experimental model rats.