Ara
Toplam kayıt 22, listelenen: 11-20
Effects of neurotrophic factors cdnf and manf on brain plasticity and repair after brain ischemia
(Wiley-Blackwell, 2016)
...
Effects of circadian rhythm on brain injury and related molecular mechanisims
(Wiley-Blackwell, 2016)
...
Investigation the effects of memantin and melatonin treatment after traumatic brain injury in mice
(Springer Heidelberg, 2014)
…
Particular phosphorylation of PI3K/Akt on Thr308 via PDK-1 and PTEN mediates melatonin's neuroprotective activity after focal cerebral ischemia in mice
(Elsevier Sciences Bv, 2017)
Apart from its potent antioxidant property, recent studies have revealed that melatonin promotes PI3K/Akt phosphorylation following focal cerebral ischemia (FCI) in mice. However, it is not clear (i) whether increased ...
Effects of normobaric oxygen and melatonin on reperfusion injury: Role of cerebral microcirculation
(Impact Journals, 2015)
In order to protect the brain before an irreversible injury occurs, penumbral oxygenation is the primary goal of current acute ischemic stroke treatment. However, hyperoxia treatment remains controversial due to the risk ...
Evidence that melatonin downregulates Nedd4-1 E3 ligase and its role in cellular survival
(Academic Press Inc Elsevier Science, 2019)
Indolamine melatonin structurally resembles non-covalent proteasome inhibitors; however, the role of ubiquitin proteasome system (UPS) in neuronal survival and how melatonin carries out UPS inhibition remain largely unknown. ...
Time dependent impact of perinatal hypoxia on growth hormone, insulin-like growth factor 1 and insulin-like growth factor binding protein-3
(Springer/Plenum Publishers, 2016)
Hypoxic-ischemia (HI) is a widely used animal model to mimic the preterm or perinatal sublethal hypoxia, including hypoxic-ischemic encephalopathy. It causes diffuse neurodegeneration in the brain and results in mental ...
Targeting different pathophysiological events after traumatic brain injury in mice: Role of melatonin and memantine
(Elsevier Ireland Ltd, 2016)
The tissue damage that emerges during traumatic brain injury (TBI) is a consequence of a variety of pathophysiological events, including free radical generation and over-activation of N-methyl-D-aspartate-type glutamate ...