1. The effects of d-allose on transient ischemic neuronal death and analysis of its mechanism
- Author
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Richard F. Keep, Tetsuhiko Toyoshima, Yanan Liu, Takashi Tamiya, Aya Shinomiya, Toshifumi Itano, Masaaki Tokuda, and Takehiro Nakamura
- Subjects
Male ,medicine.medical_specialty ,Time Factors ,Microdialysis ,Ischemia ,Glutamic Acid ,Hippocampus ,Brain damage ,Gerbil ,medicine.disease_cause ,Neuroprotection ,Drug Administration Schedule ,Internal medicine ,medicine ,Animals ,Lactic Acid ,Cerebral Cortex ,Neurons ,Analysis of Variance ,Movement Disorders ,business.industry ,General Neuroscience ,Glutamate receptor ,Deoxyguanosine ,medicine.disease ,Oxygen ,Disease Models, Animal ,Glucose ,Endocrinology ,8-Hydroxy-2'-Deoxyguanosine ,Ischemic Attack, Transient ,Anesthesia ,medicine.symptom ,Gerbillinae ,business ,Reperfusion injury ,Oxidative stress ,DNA Damage - Abstract
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 POâ‚‚ 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.
- Published
- 2014
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