The Beneficial Effect of Melatonin in Brain Endothelial Cells against Oxygen-Glucose Deprivation Followed by Reperfusion-Induced Injury
Copyright policy )The Beneficial Effect of Melatonin in Brain Endothelial Cells against Oxygen-Glucose Deprivation Followed by Reperfusion-Induced Injury
Melatonin has a cellular protective effect in cerebrovascular and neurodegenerative diseases. Protection of brain endothelial cells against hypoxia and oxidative stress is important for treatment of central nervous system (CNS) diseases, since brain endothelial cells constitute the blood brain barrier (BBB). In the present study, we investigated the protective effect of melatonin against oxygen-glucose deprivation, followed by reperfusion- (OGD/R-) induced injury, in bEnd.3 cells. The effect of melatonin was examined by western blot analysis, cell viability assays, measurement of intracellular reactive oxygen species (ROS), and immunocytochemistry (ICC). Our results showed that treatment with melatonin prevents cell death and degradation of tight junction protein in the setting of OGD/R-induced injury. In response to OGD/R injury of bEnd.3 cells, melatonin activates Akt, which promotes cell survival, and attenuates phosphorylation of JNK, which triggers apoptosis. Thus, melatonin protects bEnd.3 cells against OGD/R-induced injury.
- Seoul National University Korea (Republic of)
- Seoul National University College of Medicine Korea (Republic of)
- Yonsei University Korea (Republic of)
- New Generation University College Ethiopia
- Yonsei University College of Medicine
Vascular Endothelial Growth Factor A, 610, Gene Expression, Apoptosis, Apoptosis/drug effects*, Gene Expression/drug effects, Antioxidants, Cell Line, Reperfusion Injury/metabolism, Mice, Reactive Oxygen Species/metabolism, Proto-Oncogene Proteins c-akt/metabolism, Animals, Hypoxia, Endothelial Cells/drug effects, Melatonin, bcl-2-Associated X Protein, JNK Mitogen-Activated Protein Kinases/metabolism, Glucose/pharmacology*, Tight Junction Proteins, Melatonin/pharmacology*, Vascular Endothelial Growth Factor A/metabolism, JNK Mitogen-Activated Protein Kinases, Brain, Endothelial Cells, Glucose, Antioxidants/pharmacology, Brain/cytology, Endothelial Cells/metabolism*, bcl-2-Associated X Protein/metabolism, Reperfusion Injury, Reperfusion Injury/pathology, Tight Junction Proteins/metabolism, Reactive Oxygen Species, Endothelial Cells/cytology, Proto-Oncogene Proteins c-akt, Research Article
Vascular Endothelial Growth Factor A, 610, Gene Expression, Apoptosis, Apoptosis/drug effects*, Gene Expression/drug effects, Antioxidants, Cell Line, Reperfusion Injury/metabolism, Mice, Reactive Oxygen Species/metabolism, Proto-Oncogene Proteins c-akt/metabolism, Animals, Hypoxia, Endothelial Cells/drug effects, Melatonin, bcl-2-Associated X Protein, JNK Mitogen-Activated Protein Kinases/metabolism, Glucose/pharmacology*, Tight Junction Proteins, Melatonin/pharmacology*, Vascular Endothelial Growth Factor A/metabolism, JNK Mitogen-Activated Protein Kinases, Brain, Endothelial Cells, Glucose, Antioxidants/pharmacology, Brain/cytology, Endothelial Cells/metabolism*, bcl-2-Associated X Protein/metabolism, Reperfusion Injury, Reperfusion Injury/pathology, Tight Junction Proteins/metabolism, Reactive Oxygen Species, Endothelial Cells/cytology, Proto-Oncogene Proteins c-akt, Research Article
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