Brain-derived neurotrophic factor alleviates the oxidative stress induced by oxygen and glucose deprivation in an ex vivo brain slice model.
Paloma González-RodríguezIrene F UgidosDiego Pérez-RodríguezBerta Anuncibay-SotoMaría Santos-GaldianoEnrique Font-BelmonteJosé Manuel Gonzalo-OrdenArsenio Fernández-LópezPublished in: Journal of cellular physiology (2018)
Brain-derived neurotrophic factor (BDNF) is considered as a putative therapeutic agent against stroke. Since BDNF role on oxidative stress is uncertain, we have studied this role in a rat brain slice ischemia model, which allows BDNF reaching the neural parenchyma. Hippocampal and cerebral cortex slices were subjected to oxygen and glucose deprivation (OGD) and then returned to normoxic conditions (reperfusion-like, RL). OGD/RL increased a number of parameters mirroring oxidative stress in the hippocampus that were reduced by the BDNF presence. BDNF also reduced the OGD/RL-increased activity in a number of antioxidant enzymes in the hippocampus but no effects were observed in the cerebral cortex. In general, we conclude that alleviation of oxidative stress by BDNF in OGD/RL-exposed slices relies on decreasing cPLA2 activity, rather than modifying antioxidant enzyme activities. Moreover, a role for the oxidative stress in the differential ischemic vulnerability of cerebral cortex and hippocampus is also supported.
Keyphrases
- cerebral ischemia
- oxidative stress
- subarachnoid hemorrhage
- stress induced
- blood brain barrier
- brain injury
- ischemia reperfusion injury
- diabetic rats
- dna damage
- induced apoptosis
- functional connectivity
- blood glucose
- climate change
- type diabetes
- multiple sclerosis
- atrial fibrillation
- acute coronary syndrome
- magnetic resonance
- adipose tissue
- cognitive impairment
- acute myocardial infarction
- signaling pathway
- solid state
- endoplasmic reticulum stress