2016
DOI: 10.1590/1414-431x20165187
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Effect of hyperbaric oxygenation on mitochondrial function of neuronal cells in the cortex of neonatal rats after hypoxic-ischemic brain damage

Abstract: The timing and mechanisms of protection by hyperbaric oxygenation (HBO) in hypoxic-ischemic brain damage (HIBD) have only been partially elucidated. We monitored the effect of HBO on the mitochondrial function of neuronal cells in the cerebral cortex of neonatal rats after HIBD. Neonatal Sprague-Dawley rats (total of 360 of both genders) were randomly divided into normal control, HIBD, and HIBD+HBO groups. The HBO treatment began immediately after hypoxia-ischemia (HI) and continued once a day for 7 consecutiv… Show more

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Cited by 11 publications
(8 citation statements)
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References 30 publications
(34 reference statements)
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“…It is well known that ischemic stroke is associated with oxidative stress and severe impairments of mitochondrial functioning in the damaged brain region [ 35 ]. Numerous studies have demonstrated that the protection of the mitochondria of neural cells from damage can be an effective therapeutic approach for the treatment of acute neurological disorders [ 36 , 37 , 38 , 39 ]. Most of these strategies consisted in either antioxidant usage to decrease excessive levels of ROS or in the induction of signaling cascades associated with preconditioning that ultimately prevented the increase of mitochondrial permeability.…”
Section: Discussionmentioning
confidence: 99%
“…It is well known that ischemic stroke is associated with oxidative stress and severe impairments of mitochondrial functioning in the damaged brain region [ 35 ]. Numerous studies have demonstrated that the protection of the mitochondria of neural cells from damage can be an effective therapeutic approach for the treatment of acute neurological disorders [ 36 , 37 , 38 , 39 ]. Most of these strategies consisted in either antioxidant usage to decrease excessive levels of ROS or in the induction of signaling cascades associated with preconditioning that ultimately prevented the increase of mitochondrial permeability.…”
Section: Discussionmentioning
confidence: 99%
“…Mitochondrial dysfunction stands as a therapeutic target in stroke and TBI due to its role in the secondary injury mechanism. 41,42 However, HBOT as a treatment for cerebrovascular diseases has yielded mixed results. 14 The initiation of HBOT may dictate the therapeutic, or detrimental, outcomes.…”
Section: Discussionmentioning
confidence: 99%
“…Hypoxic–ischemic encephalopathy (HIE) is a severe brain disease with high morbidity and mortality worldwide 1 . Typically, HIE causes irreversible necrosis, cell apoptosis, and neuron death, which can lead to permanent neurological morbidity 2 . Our previous study revealed that notoginsenoside R1 (NGR1) protects the brain from hypoxic–ischemic injury through the inhibition of endoplasmic reticulum (ER) stress pathways 3 .…”
Section: Introductionmentioning
confidence: 99%