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Neuroprotective Effects of Acetyl-L-Carnitine Against Oxygen-Glucose Deprivation-Induced Neural Stem Cell Death.
Mol Neurobiol. 2016 12; 53(10):6644-6652.MN

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.

Authors+Show Affiliations

Department of Translational Medicine, Hanyang University Graduate School of Biomedical Science & Engineering, Seoul, Republic of Korea.Department of Neurology, Hanyang University College of Medicine, Seoul, Republic of Korea.Department of Neurology, Hanyang University College of Medicine, Seoul, Republic of Korea.Department of Neurology, Hanyang University College of Medicine, Seoul, Republic of Korea.Department of Neurology, Hanyang University College of Medicine, Seoul, Republic of Korea.Department of Chemistry and Research Institute of Natural Sciences, Hanyang University, 222 Wangsimni-ro, Seongdong-gu, Seoul, 133-791, Republic of Korea.Department of Translational Medicine, Hanyang University Graduate School of Biomedical Science & Engineering, Seoul, Republic of Korea. ksh213@hanyang.ac.kr. Department of Neurology, Hanyang University College of Medicine, Seoul, Republic of Korea. ksh213@hanyang.ac.kr. Department of Neurology, Hanyang University College of Medicine, 249-1 Guri Hospital, Gyomun-dong, Guri-si, Gyeonggi-do, 471-701, Republic of Korea. ksh213@hanyang.ac.kr.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

26643543

Citation

Bak, Seong Wan, et al. "Neuroprotective Effects of Acetyl-L-Carnitine Against Oxygen-Glucose Deprivation-Induced Neural Stem Cell Death." Molecular Neurobiology, vol. 53, no. 10, 2016, pp. 6644-6652.
Bak SW, Choi H, Park HH, et al. Neuroprotective Effects of Acetyl-L-Carnitine Against Oxygen-Glucose Deprivation-Induced Neural Stem Cell Death. Mol Neurobiol. 2016;53(10):6644-6652.
Bak, S. W., Choi, H., Park, H. H., Lee, K. Y., Lee, Y. J., Yoon, M. Y., & Koh, S. H. (2016). Neuroprotective Effects of Acetyl-L-Carnitine Against Oxygen-Glucose Deprivation-Induced Neural Stem Cell Death. Molecular Neurobiology, 53(10), 6644-6652.
Bak SW, et al. Neuroprotective Effects of Acetyl-L-Carnitine Against Oxygen-Glucose Deprivation-Induced Neural Stem Cell Death. Mol Neurobiol. 2016;53(10):6644-6652. PubMed PMID: 26643543.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Neuroprotective Effects of Acetyl-L-Carnitine Against Oxygen-Glucose Deprivation-Induced Neural Stem Cell Death. AU - Bak,Seong Wan, AU - Choi,Hojin, AU - Park,Hyun-Hee, AU - Lee,Kyu-Yong, AU - Lee,Young Joo, AU - Yoon,Moon-Young, AU - Koh,Seong-Ho, Y1 - 2015/12/08/ PY - 2015/07/12/received PY - 2015/11/29/accepted PY - 2015/12/9/pubmed PY - 2017/12/30/medline PY - 2015/12/9/entrez KW - Acetyl-L-carnitine KW - Oxygen glucose deprivation KW - Phosphatidylinositol 3-kinase KW - Stroke SP - 6644 EP - 6652 JF - Molecular neurobiology JO - Mol. Neurobiol. VL - 53 IS - 10 N2 - 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. SN - 1559-1182 UR - https://www.unboundmedicine.com/medline/citation/26643543/Neuroprotective_Effects_of_Acetyl_L_Carnitine_Against_Oxygen_Glucose_Deprivation_Induced_Neural_Stem_Cell_Death_ L2 - https://dx.doi.org/10.1007/s12035-015-9563-x DB - PRIME DP - Unbound Medicine ER -