动物造模,缺氧缺血性脑病 z-bio 2021-09-08 775

　　Objective: To explore the effect of edaravone on cerebral edema and CD163/HO-1 signaling pathway in neonatal rats with hypoxic-ischemic encephalopathy (HIE).

　　Methods: 120 7-day-old SD neonatal rats, 90 of which were double-ligated the left common carotid artery and hypoxia were used to make hypoxic ischemic brain damage (HIBD) models, and were randomly divided into model groups. In the daravone group, the other 30 animals were treated as a sham operation group with only threading, no ligation and no hypoxia. The edaravone group was injected intraperitoneally with 2 mg/kg of edaravone immediately after the model was made, once a day for 5 consecutive days; model group Both the sham operation group and the sham operation group were given intraperitoneal injections of the same amount of normal saline at the same time. After the operation, observe the biological behavior of the SD newborn rats in each group. 24 hours after modeling, TTC staining was used to observe the brain tissue morphology of the SD newborn rats in each group. After the simulation, the water content of the brain tissue of SD neonatal rats in each group was detected at 6h, 12h, 24h, 2d, 3d, 5d; fluorescence quantitative PCR (qRT-PCR) technology was used to detect the expression level of CD163 and HO-1 mRNA; Westernblot technology was used to detect CD163 ､HO-1 protein expression level.

　　Results: 90 SD neonatal rats developed symptoms such as lethargy, lethargy, and convulsions after the operation. After treatment with edaravone, the symptoms were significantly reduced compared with the model group, and the symptoms were improved within 3 days. TTC staining found that the neonatal rats in the model group 24h after modeling Edema appeared in the left hemisphere, pale in color, and slightly larger in volume than the right hemisphere. After edaravone treatment, the degree of brain tissue damage was significantly reduced. The infarct area of the left hemisphere of the neonatal rat in the model group and the edaravone group was significantly larger than that in the sham operation group (P<0.05), the area of cerebral infarction after edaravone treatment was significantly smaller than that in the model group (P<0.05). Brain tissue water content test results showed: 6h after modeling, the brain tissue of newborn rats in the model group and edaravone group The water content was significantly higher than that of the sham operation group (P<0.05), and the brain water content was the highest at 2 days. The brain water content of neonatal rats after edaravone treatment was significantly lower than that of the model group (P<0.05). qRT-PCR and Western blot results showed that compared with the sham operation group, the expression of CD163 and HO-1 mRNA and protein in the brain tissue of the model group and the edaravone group was significantly increased (P<0.05). After edaravone treatment The expression levels of CD163 and HO-1 mRNA and protein in neonatal rats were significantly higher than those in the model group (P<0.05).

　　Conclusion: Edaravone can significantly reduce cerebral edema and cerebral infarction in HIBD neonatal rats, and its mechanism may be related to the activation of CD163/HO-1 signaling pathway.