| BackgroundCerebral infarction,also known as ischemic stroke,refers to a kind of clinical synthesis of brain blood supply disorders caused by various causes,leading to regional brain ischemia and hypoxic necrosis,and corresponding neurological deficits.Sign.Ischemic stroke is the most common type of stroke,accounting for 70%~80%.The local inflammatory response is first caused by stroke,and the inflammatory response around the stroke site is more serious than the stroke itself.In recent years,it has been found that the Nrf2/ARE pathway,which is based on the nuclear factor erythroid 2-related factor(Nrf2),plays an important role in regulating cellular inflammatory responses.However,the specific role of Nrf2 in ischemic stroke is currently less reported,and the specific mechanism remains unclear.ObjectivesIntracerebral artery occlusion and Nrf2 agonist in rats resulted in an increase in Nrf2 expression,and a rat model of Nrf2 overexpression after ischemia-reperfusion was established to observe brain tissue in rats with high reperfusion of Nrf2.Changes in protein expression levels of pro-inflammatory cytokines(IFN,IL-6)and protein expression levels of astrocyte and microglial activation markers(GFAP,Iba-1),and observation of Nrf2 deficiency in brain tissue The change of blood infarct size,the effect of Nrf2 on the inflammatory response of ischemia-reperfusion and the mechanism of action in ischemic stroke disease.Methods1.Healthy adult SD male rats were randomly divided into normal group,shamoperation group,stroke obstruction side group,stroke obstruction contralateral group,Nrf2 agonist group and blank solvent control group,with 5 rats in each group.The middle cerebral artery occlusion method(MCAO)operation was performed on the stroke obstruction side group,the stroke obstruction contralateral group,the Nrf2 agonist group,and the blank solvent control group.The Nrf2 agonist group and the blank solvent control group were given one day after the operation.Stroke rats were injected with Nrf2 agonist and saline respectively.2.Three days after modeling,the expression of inflammatory factors(IL-6,IFN)in the brain of rats in the normal group,sham operation group,stroke obstruction group and stroke obstruction group was detected by western-blot technique.3.The expression of Nrf2 in the sham operation group,the stroke obstruction group and the Nrf2 agonist group was detected by western-blot technique 3 days after modeling.4.Three days after model establishment,the normal group,sham operation group,stroke obstruction side group,Nrf2 agonist group,solvent control group brain tissue inflammatory factors(IL-6,IFN)and microglia(Iba)were detected by western-blot technique.-1)Expression of astrocyte activation marker(GFAP).5.The volume of cerebral infarction was observed by TTC staining technique in rats in the stroke group and Nrf2 agonist group.6.In this experiment,SPSS 20.0 software was used to analyze the experimental data.The measurement data were expressed as mean ± standard deviation().The two groups were compared using independent sample t test.The comparison between groups of samples was based on one-way ANOVA.In the analysis,the LSD method was used to compare the variances between groups,and the Tamhane method was used when the variance was not uniform.The test results were considered statistically significant when P< 0.05.Results1.Three days after surgery,the expression levels of inflammatory factors(IL-6,IFN)in the brain tissue of the rats in the stroke obstruction group were significantly higher than those in the normal group,the sham operation group and the contralateral side of the stroke obstruction,P < 0.05 was statistically significant.2.The expression level of Nrf2 in the brain tissue of the rats with stroke obstruction was significantly higher than that of the sham operation group,P < 0.05 was statistically significant.3.The expression levels of inflammatory cytokines(IL-6,IFN)in brain tissue of rats in Nrf2 agonist group were significantly lower than those in stroke obstruction group,P <0.05 was statistically significant;glial cell activation markers(Iba-1,GFAP)The expression level decreased significantly,P < 0.05 was statistically significant.4.TTC staining results showed that the infarct volume of the Nrf2 agonist group was significantly higher than that of the stroke group,P < 0.05 was statistically significant.ConclusionsIschemia-reperfusion induces central nervous system inflammation in rats,causing damage to the nervous system.Increased expression of Nrf2 can inhibit the activation of glial cells in brain tissue by activating Nrf2/ARE signaling pathway,reduce inflammation levels,thereby reducing the area of infarcts,promoting reperfusion of infarcted brain tissue,and improving brain ischemia-reperfusion injury.. |
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