Dexamethasone has been reported to reduce the infarct volume and protect neurological function after ischaemic injury, but the mechanism of Dex in brain injury is not clear. We aimed to study the mechanism by which dexamethasone protects against ischaemic brain injury. Western blotting was to detected the expression of Hap1,TrkB, Akt and Erk; TTC staining to analyse ischemic volume; neurological deficit evaluation to test degree of ischemic injury; immunofluorescence staining to analyse the distribution of Hap1; and the MCAO model was used to study these processes. All data are expressed as the means ± SEM and were analysed by GraphPad Prism 6. P < 0.05 was considered statistically significant. After dexamethasone (Dex) treatment, Hap1 levels were increased and peaked at 2 days; then, we found that body weight was decreased in Hap1-/+ mice. Further study showed that Dex treatment reduced the ischaemic volume and improved neurological function. Finally, we showed that Hap1 regulated the levels of pTrkB, pAkt and pErk 1/2 in ischaemic injury after Dex treatment. Our data suggest that dexamethasone protects against ischaemic brain injury by inhibiting the pAkt signalling pathway through increasing Hap1.
Keywords: Akt; Dexamethasone; Hap1; Stroke.