The beneficial effect of melatonin in brain endothelial cells against oxygen-glucose deprivation followed by reperfusion-induced injury.
Juhyun SongSo Mang KangWon Taek LeeKyung Ah ParkKyoung Min LeeJong Eun LeePublished in: Oxidative medicine and cellular longevity (2014)
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.
Keyphrases
- high glucose
- endothelial cells
- cell cycle arrest
- cell death
- induced apoptosis
- oxidative stress
- diabetic rats
- reactive oxygen species
- endoplasmic reticulum stress
- cerebral ischemia
- blood brain barrier
- signaling pathway
- acute myocardial infarction
- pi k akt
- heart failure
- resting state
- adipose tissue
- drug induced
- high throughput
- coronary artery disease
- blood glucose
- acute coronary syndrome
- high resolution
- small molecule
- skeletal muscle
- subarachnoid hemorrhage
- left ventricular
- replacement therapy
- single molecule
- combination therapy
- smoking cessation
- weight loss
- protein kinase