The Beneficial Effect of Melatonin in Brain Endothelial Cells against Oxygen-Glucose Deprivation Followed by Reperfusion-Induced Injury

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Authors: Juhyun Song ; So Mang Kang ; Won Taek Lee ; Kyung Ah Park ; Kyoung Min Lee ; Jong Eun Lee

Citation: OXIDATIVE MEDICINE AND CELLULAR LONGEVITY, Vol.2014 : 639531, 2014

MeSH: Animals ; Antioxidants/pharmacology ; Apoptosis/drug effects* ; Brain/cytology ; Cell Line ; Endothelial Cells/cytology ; Endothelial Cells/drug effects ; Endothelial Cells/metabolism* ; Gene Expression/drug effects ; Glucose/pharmacology* ; Hypoxia ; JNK Mitogen-Activated Protein Kinases/metabolism ; Melatonin/pharmacology* ; Mice ; Proto-Oncogene Proteins c-akt/metabolism ; Reactive Oxygen Species/metabolism ; Reperfusion Injury/metabolism ; Reperfusion Injury/pathology ; Tight Junction Proteins/metabolism ; Vascular Endothelial Growth Factor A/metabolism ; bcl-2-Associated X Protein/metabolism

Abstract: 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.