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 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.
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Authors | Yanan Liu, Takehiro Nakamura, Tetsuhiko Toyoshima, Aya Shinomiya, Takashi Tamiya, Masaaki Tokuda, Richard F Keep, Toshifumi Itano |
Journal | Brain research bulletin
(Brain Res Bull)
Vol. 109
Pg. 127-31
(Oct 2014)
ISSN: 1873-2747 [Electronic] United States |
PMID | 25445611
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2014 Elsevier Inc. All rights reserved. |
Chemical References |
- Lactic Acid
- Glutamic Acid
- allose
- 8-Hydroxy-2'-Deoxyguanosine
- Deoxyguanosine
- Glucose
- Oxygen
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Topics |
- 8-Hydroxy-2'-Deoxyguanosine
- Analysis of Variance
- Animals
- Cerebral Cortex
(drug effects, metabolism, pathology)
- DNA Damage
(drug effects)
- Deoxyguanosine
(analogs & derivatives)
- Disease Models, Animal
- Drug Administration Schedule
- Gerbillinae
- Glucose
(pharmacology, therapeutic use)
- Glutamic Acid
(metabolism)
- Ischemic Attack, Transient
(complications, drug therapy, pathology)
- Lactic Acid
(metabolism)
- Male
- Microdialysis
- Movement Disorders
(etiology)
- Neurons
(drug effects)
- Oxygen
(metabolism)
- Time Factors
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