Dexmedetomidine Attenuates Hippocampal Damage and Improves Cognition by Up-Regulating Glyoxalase1 in APP/PS1 Mice

Background: Dexmedetomidine (DEX), an α2-adrenoceptor agonist, has been reported to possess neuroprotective effects against postoperative cognitive impairment. GLO-1 plays a key role in the pathogenesis of Alzheimer’s disease (AD). Here, the primary goal was to assess whether DEX affect GLO-1 and protect cognition impairment in APP/PS1 transgenic mice.Methods: After DEX was intraperitoneally injected in APP/PS1 mice, behavior was tested by Water Maze to illustrate whether DEX treatment has a significantly positive effect on ameliorating the cognition deficits in AD. We assessed the effect of DEX on the expression of GLO-1 and the production of other oxidative stress factors by ELISA and Western blot. To determine whether DEX play roles in the Aβ induced neuron apoptosis, flow cytometry was used.Results: DEX treatment significantly ameliorated cognition deficits in APP/PS1 mice. DEX increased GLO-1 expression and decreased MG activity in the hippocampus. In addition, DEX increased activity of SOD, GSH and reduced the activity of MDA. In vitro, DEX could protect the neuron apoptosis induced by Aβ. GLO-1 inhibitor could block the protective role of DEX.Conclusion: Taken together, our findings suggest that DEX prevents progression of AD-like pathology through upregulating GLO-1.