Abstract | BACKGROUND:
2-Deoxy-D-glucose is an inhibitor of glycolysis, which is protective in animal models of brain pathology, but the mechanisms of this protection are unclear. We examined whether, when and how deoxyglucose protects neurons in co-culture with astrocytes and microglia. Microglia are brain macrophages, which can damage neurons in inflammatory conditions. METHODS:
Deoxyglucose was added to primary cultures of microglia and astrocytes from rat cortex, or neurons and glia from rat cerebellum, or the BV-2 microglial cell line, and cell death and cell functions were evaluated. RESULTS: CONCLUSIONS: We conclude that deoxyglucose causes microglial loss by ATP depletion, and this can protect neurons from neurodegeneration, except in conditions of hypoxia. Deoxyglucose may thus be beneficial in brain pathologies mediated by microglia, including brain trauma, but not where hypoxia is involved.
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Authors | Anna Vilalta, Guy C Brown |
Journal | Journal of neuroinflammation
(J Neuroinflammation)
Vol. 11
Pg. 58
(Mar 26 2014)
ISSN: 1742-2094 [Electronic] England |
PMID | 24669778
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Amyloid beta-Peptides
- Neuroprotective Agents
- Tumor Necrosis Factor-alpha
- Deoxyglucose
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Topics |
- Amyloid beta-Peptides
(toxicity)
- Animals
- Animals, Newborn
- Cell Count
- Cell Death
(drug effects)
- Cells, Cultured
- Cerebellum
(cytology)
- Deoxyglucose
(pharmacology)
- Female
- Hypoxia
(drug therapy)
- Male
- Microglia
(physiology)
- Neurons
(drug effects)
- Neuroprotective Agents
(pharmacology)
- Phagocytosis
(drug effects)
- Rats, Wistar
- Time Factors
- Tumor Necrosis Factor-alpha
(metabolism)
- Wounds and Injuries
(drug therapy, prevention & control)
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