Mechanism Of GSK3?/STAT3 After Hypoxic Preconditioning In Rats With Ischemic Brain Injury

Objective: To investigate the expression of GSK3?(Ser9)and /STAT3(Tyr705)in ischemic brain injury in rats,to explore the GSK3? inhibitor and hypoxia preconditioning neuroprotection on ischemic brain injury in rats and its possible mechanism.Methods: The 120 male SD SPF rats were randomly divided into normal group(N,20 rats),sham operation group(M,20 rats),cerebral infarction group(M,20 rats),hypoxia preconditioning + cerebral infarction group(HM,20 rats),hypoxic preconditioning + the cerebral infarction + saline group(HMN,20 rats),hypoxia preconditioning + cerebral infarction + inhibitor group(HMI,20 rats),the establishment of middle cerebral artery occlusion model with modified Longa line embolism method(MCAO),The neurological function score was performed 24 hours after modeling successful;cerebral infarction volume was measured by TTC staining;the expression of NeuN and p-STAT3 in the Cerebral cortex were detected by immunohistochemical chemical method;the expression of pGSK3?(Ser9)and pSTAT3(Tyr705)positive cells were detected by Western blot method,the relative expression of inflammatory cytokines IL-10,TNF-? was detected by RT-PCR in brain tissue of rats.Results: Compared with the group M,the neurological function score and infarct volume of group HM and group HMI were significantly lower(P <0.05).Compared with the group M,the expression of NeuN of group HM and group HMI were increased,however the expression of pGSK3?(Ser9)and pSTAT3(Tyr705)positive cells were significantly decreased(P <0.05).Compared with the simple infarctiongroup,the expression of TNF-a of group HM and group HMI were significantly decreased(P <0.05),The expression of IL-10 was up-regulated after cerebral infarction.There was significant difference between group HM and group HMI(P <0.05)Conclusions: Hypoxia preconditioning has protective effect on ischemic brain injury in rats,which can alleviate the symptoms of neurological deficit,reduce infarct volume.After ischemic brain injury in rats,which can increase the expression of pGSK3?(Ser9)and pSTAT3(Tyr705),at the same time decrease the expression of NeuN.After the application of pGSK3?(Ser9)specific inhibitor and after hypoxia preconditioning,which can reduce the expression of pGSK3?(Ser9)and pSTAT3(Tyr705),in the mean while increase the expression of NeuN.Among them,the group HM doesn't change significantly in the group HMI.Moreover,compared with group M,in group HMI and HM.The release of proinflammatory cytokines TNF-a decreases significantly,however the expression of anti-inflammatory factor IL-10 increases,Neurological deficit symptoms improve significantly,which plays a protective role in the superposition of neural function.