Research reportThe effects of d-allose on transient ischemic neuronal death and analysis of its mechanism

- d-Allose, a rare sugar, significantly reduced cerebral ischemia/reperfusion-induced hippocampal neuronal death.
- d-Allose significantly attenuated ischemia-induced motor hyperactivity.
- The protection was associated with reduced extracellular glutamate and lactate, as well as less oxidative damage.

The present study investigates the neuroprotective effects of d-allose, a rare sugar, against ischemia/reperfusion injury in a gerbil model. Transient forebrain ischemia was induced by occlusion of the bilateral common carotid arteries for 5 min. d-Allose was intravenously injected before and after ischemia (200 mg/kg). Extracellular glutamate and lactate release from the gerbil brain, and PO2 profiles were monitored during ischemia and reperfusion. We also examined neuronal death and oxidative damage in the hippocampus one week after ischemia reperfusion, and investigated functional outcome. d-Allose administration suppressed glutamate and lactate release compared to vehicle controls. Brain damage, 8-OHdG levels (a marker of oxidative stress) and locomotor activities were significantly decreased by d-allose treatment. The present results suggest that d-allose reduces delayed neuronal death and behavioral deficits after transient ischemia by changing cerebral metabolism and inhibiting oxidative stress.