The Effect Of Sevoflurane-pretreatment For GFAP Expression Of Focal Cerebral Ischemia-reperfusion Injury In Rats

Background: Ischemia-reperfusion injury refers to a condition that it is not only that tissue and organ function can restore function after reperfusion, but it can cause structural damage. More and more attention has been paid on its pathogenesis, the star-colloid cells in the cerebral ischemia in the role of growing concern. In recent years, the role of astrocytes in prevention to brain ischemia reperfusion has been one of concerns GFAP (glial fibrillary acid protein, GFAP) is the main unit of brain glial fibers and a marker of astrocytes (astrocytes, AST). GFAP expression will change once nervous tissue ischemic injury occurs. Researches have found that inhaled anesthetics (enflurane, isoflurane) preconditioning has protective effects on brain systems. Whether sevoflurane, a new inhalation anesthetic widely used in clinical anesthesia, can reduce cerebral ischemia reperfusion injury, its mechanism deserves further study and discussion.Objective:To study the expression change of GFAP after sevoflurane reconditioning and focal cerebral ischemia-reperfusion injury.Methods:The sevoflurane preconditioning model and PMCAO model were made ,128 rats were randomly divided into 4 groups: control group (control), 2.2% sevoflurane treatment group (SEVO), ischemia-reperfusion group (PMCAO), 2.2% sevoflurane preconditioning (SEVO) + PMCAO group, n = 32. 6h, 24h, 48h, 72h, sub-4 time points after reperfusion injury ,8.rats were killed and observed each time,and the expression of GFAP was examined by immunofluorescence staining at 6 h, 24h, 48h, 72h after cerebral ischemia/ reperfusion.Results:There was not significant different between control group and the sevoflurane group in glial fibrillary acidic protein (GFAP) expression After reperfusion, the expression of GFAP gradually increased and peaked at 24h after ischemia. In the isoflurane preconditioning 2h +focal cerebral ischemia group, the expression of GFAP increased significantly in the infarct border compared with ischemia control group (PMCAO) (P<0.05) .Conclusion:The activation and proliferation of astrocytes was significantly suppressed by sevoflurane-preconditioning, which might be one of the protective mechanisms of focal cerebral ischemia-reperfusion injury.