Abstract
Brain ischemic postconditioning is the induction of brief periods of ischemia–reperfusion during the early stages following ischemia, and it has been shown to produce neuroprotective effects. The mechanisms underlying these neuroprotective effects are poorly understood. Glutamate excitotoxicity is one cause of postischemic neuronal death. Glutamine synthetase (GS) is an enzyme that is expressed in glial cells and may affect glutamate excitotoxicity. We induced global ischemia in rats and performed postconditioning with 6 cycles of 10 seconds reperfusion and 10 seconds reocclusion before final reperfusion. Hematoxylin and eosin staining revealed extensive neuronal loss (44.0 ± 2.8% cell survival) in the hippocampal CA1 region. Ischemic postconditioning decreased neuronal death (82.0 ± 5.6% cell survival; p < 0.05). Western blotting revealed significantly increased GS expression in the hippocampus for the ischemia–reperfusion group over time compared with the sham group ( p < 0.05). Ischemic postconditioning resulted in significantly increased ( p < 0.05) GS expression compared with both the sham and ischemia–reperfusion groups, suggesting that upregulation of GS expression after ischemia constitutes a neuroprotective mechanism.
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