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Brain‐derived neurotrophic factor alleviates the oxidative stress induced by oxygen and glucose deprivation in an ex vivo brain slice model
Author(s) -
GonzálezRodríguez Paloma,
Ugidos Irene F.,
PérezRodríguez Diego,
AnuncibaySoto Berta,
SantosGaldiano María,
FontBelmonte Enrique,
GonzaloOrden José Manuel,
FernándezLópez Arsenio
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.27646
Subject(s) - oxidative stress , hippocampus , neurotrophic factors , hippocampal formation , brain derived neurotrophic factor , cerebral cortex , ex vivo , chemistry , endocrinology , neuroscience , medicine , biology , biochemistry , in vitro , receptor
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.