Hyperbaric oxygen treatment: the influence on the hippocampal superoxide dismutase and Na+,K+-ATPase activities in global cerebral ischemia-exposed rats

Mršić-Pelčić, Jasenka; Pelčić, Goran; Vitezić, Dinko; Antončić, Igor; Filipović, Tatjana; Simonić, Ante; Župan, Gordana

doi:10.1016/j.neuint.2003.10.004

Cited by 37 publications

(11 citation statements)

References 42 publications

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“…In the acute phase (day 1), HBO also prevented a decrease in SOD-1 ( P < 0.05), which protects cells against oxidative-stress (Chan et al, 1994; Nishi et al, 2005). HBO-enhanced SOD-1 activity during particular periods of reperfusion has been reported in models of severe brain ischemia, indicating a potential benefit of treatment (Mrsic-Pelcic et al, 2004b). In a similar finding to ours, rats exposed to global cerebral ischemia for 20 min and treated with HBO within 6 h of reperfusion showed no change in SOD-1 expression (Mrsic-Pelcic et al, 2004a).…”

Section: Discussionmentioning

confidence: 95%

Neuroprotective Effect of Hyperbaric Oxygen Therapy on Anterior Ischemic Optic Neuropathy

Avraham-Lubin¹,

Dratviman‐Storobinsky²,

El³

et al. 2011

Front. Neur.

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The study investigated the therapeutic effect of hyperbaric oxygen (HBO) on anterior ischemic optic neuropathy in a rodent model (rAION). rAION was laser-induced in one eye of 63 mice. The fellow (uninjured) eye served as an internal control. Thirty-three mice underwent two 90-min sessions of 100% oxygen (2 atm) treatment immediately following injury and one session daily thereafter for up to 14 days. The remaining mice were untreated. Retinas were harvested at different time points, and mRNA levels of various genes were analyzed by real-time polymerase chain reaction and histologic study. Untreated mice: day 1 post-rAION – SOD-1 (oxidative-stress-related) decreased to 82% of control (uninjured eye) levels (P < 0.05), Caspase-3 (proapoptotic) decreased to 89%, Bcl-xL mildly increased (117%; all NS); day 3 – HO-1 and endothelial nitric oxide synthase (eNOS; ischaemia-related) decreased to 74%, and Bcl-2-associated X protein, Caspase-3, and B-cell lymphoma 2 (Bcl-2; apoptotic) increased by 170, 120, and 111%, respectively (all NS); day 21 – HO-1 increased to 222% (NS) and eNOS decreased to 48% (P < 0.05). Treated mice: day 1 – SOD-1 and Caspase-3 remained unchanged, Bcl-2 and Bcl-xL mildly increased (112 and 126% respectively); day 3 – HO-1 and eNOS increased, apoptosis-related gene decreased; day 21 – SOD-1 decreased whereas eNOS increased (P < 0.05), and HO-1 increased to a lesser degree than without treatment. None of the oxygen-treated animals had retinal ganglion cell loss or a decrease in Thy-1 expression. In conclusion, HBO treatment after rAION induction influences the expression of apoptosis-related genes as well as oxidative-stress-induced and ischaemia-related genes and may exert a neuroprotective effect.

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Section: Discussionmentioning

confidence: 95%

Neuroprotective Effect of Hyperbaric Oxygen Therapy on Anterior Ischemic Optic Neuropathy

Avraham-Lubin¹,

Dratviman‐Storobinsky²,

El³

et al. 2011

Front. Neur.

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“…As the primary energy user consuming half of the ATP in the brain, sodium pump activity is highly sensitive to ATP levels. Under energy deficient conditions such as hypoxia, ischemia, and stroke, NKA dysfunction is often a major early pathological response (91, 92), which leads to a loss in membrane potential and neuronal function.…”

Section: Energy Dysregulation In Ischemia and Strokementioning

confidence: 99%

Synaptic Activity and Bioenergy Homeostasis: Implications in Brain Trauma and Neurodegenerative Diseases

Khatri

Man

2013

Front. Neurol.

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Powered by glucose metabolism, the brain is the most energy-demanding organ in our body. Adequate ATP production and regulation of the metabolic processes are essential for the maintenance of synaptic transmission and neuronal function. Glutamatergic synaptic activity utilizes the largest portion of bioenergy for synaptic events including neurotransmitter synthesis, vesicle recycling, and most importantly, the postsynaptic activities leading to channel activation and rebalancing of ionic gradients. Bioenergy homeostasis is coupled with synaptic function via activities of the sodium pumps, glutamate transporters, glucose transport, and mitochondria translocation. Energy insufficiency is sensed by the AMP-activated protein kinase (AMPK), a master metabolic regulator that stimulates the catalytic process to enhance energy production. A decline in energy supply and a disruption in bioenergy homeostasis play a critical role in multiple neuropathological conditions including ischemia, stroke, and neurodegenerative diseases including Alzheimer’s disease and traumatic brain injuries.

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“…After global cerebral ischaemia, significant increase in the SOD activities was registered after both common carotid arteries occlusion for 10–20 min. and measured from 1 hr up to 7 days of reperfusion . Viggiano et al .…”

Section: Discussionmentioning

confidence: 99%

Decrease in Oxidative Stress Parameters after Post‐Ischaemic Recombinant Human Erythropoietin Administration in the Hippocampus of Rats Exposed to Focal Cerebral Ischaemia

Mršić-Pelčić

Pilipović

Pelčić

et al. 2017

Basic Clin Pharma Tox

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Recombinant human erythropoietin (rhEpo) is a multi-functional drug with antioxidant potential. However, the underlying molecular mechanisms of its action are still unclear. The purpose of this study was to investigate the effects of rhEpo on the brain infarct volume as well as on the levels of the neuronal damage, oxidative stress parameters and active caspase-3, nuclear factor erythroid 2-related factor 2 (Nrf2) and haemeoxygenase-1 (HO-1) expressions in the hippocampi of rats exposed to the right middle cerebral artery occlusion (MCAO) for 1 hr. Ischaemic animals received either vehicle or rhEpo (5000 IU/kg, i.p.) immediately or 3 hr after the induction of ischaemia. Sham-operated, vehicle-treated animals served as the control group. Rats were killed 24 hr after the onset of the ischaemic or sham experimental procedure. MCAO caused ipsilateral brain infarction within the striatum and cortex. In the CA1 region of the hippocampi, we did not find significant neuronal loss, but a statistically significant rise in the active caspase-3 and Nrf2 protein expressions was registered. We detected also significant increases in the hippocampal levels of oxidative stress parameters (thiobarbituric acid-reactive substances, superoxide dismutase, glutathione peroxidase). Post-ischaemic administration of rhEpo significantly reduced the brain infarct volume, decreased levels of all tested oxidative stress parameters and increased the Nrf2 expression level. These findings suggest that decrease in oxidative stress parameters in the hippocampus could be an early indicator of post-ischaemic neuroprotective effect of rhEpo in rats exposed to focal cerebral ischaemia and that this effect could be attributable to additional post-ischaemic activation of Nrf2 endogenous antioxidant system.

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Hyperbaric oxygen treatment: the influence on the hippocampal superoxide dismutase and Na+,K+-ATPase activities in global cerebral ischemia-exposed rats

Cited by 37 publications

References 42 publications

Neuroprotective Effect of Hyperbaric Oxygen Therapy on Anterior Ischemic Optic Neuropathy

Neuroprotective Effect of Hyperbaric Oxygen Therapy on Anterior Ischemic Optic Neuropathy

Synaptic Activity and Bioenergy Homeostasis: Implications in Brain Trauma and Neurodegenerative Diseases

Decrease in Oxidative Stress Parameters after Post‐Ischaemic Recombinant Human Erythropoietin Administration in the Hippocampus of Rats Exposed to Focal Cerebral Ischaemia

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