Abstract |
Deprivation of oxygen and glucose is the main cause of neuronal cell death during cerebral infarction and can result in severe morbidity and mortality. In general, the neuroprotective therapies that are applied after ischemic stroke have been unsuccessful, despite many investigations. Acetyl-L-carnitine ( ALCAR) plays an important role in mitochondrial metabolism and in modulating the coenzyme A ( CoA)/acyl- CoA ratio. We investigated the protective effects of ALCAR against oxygen- glucose deprivation (OGD) in neural stem cells (NSCs). We measured cell viability, proliferation, apoptosis, and intracellular signaling protein levels after treatment with varying concentrations of ALCAR under OGD for 8 h. ALCAR protected NSCs against OGD by reducing apoptosis and restoring proliferation. Its protective effects are associated with increases in the expression of survival-related proteins, such as phosphorylated Akt (pAkt), phosphorylated glycogen synthase kinase 3b (pGSK3b), B cell lymphoma 2 (Bcl-2), and Ki-67 in NSCs that were injured by OGD. ALCAR also reduced the expression of death-related proteins, such as Bax, cytosolic cytochrome C, cleaved caspase-9, and cleaved caspase-3. We concluded that ALCAR exhibits neuroprotective effects against OGD-induced damage to NSCs by enhancing the expression of survival signals and decreasing that of death signals.
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Authors | Seong Wan Bak, Hojin Choi, Hyun-Hee Park, Kyu-Yong Lee, Young Joo Lee, Moon-Young Yoon, Seong-Ho Koh |
Journal | Molecular neurobiology
(Mol Neurobiol)
Vol. 53
Issue 10
Pg. 6644-6652
(12 2016)
ISSN: 1559-1182 [Electronic] United States |
PMID | 26643543
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Neuroprotective Agents
- Acetylcarnitine
- Glucose
- Oxygen
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Topics |
- Acetylcarnitine
(pharmacology)
- Animals
- Cell Death
(drug effects)
- Cell Proliferation
(drug effects)
- Cell Survival
(drug effects)
- Glucose
(deficiency)
- Intracellular Space
(metabolism)
- Neural Stem Cells
(drug effects, metabolism, pathology)
- Neuroprotective Agents
(pharmacology)
- Oxygen
(metabolism)
- Rats
- Signal Transduction
(drug effects)
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