Mechanism of ischemic tolerance induced by hyperbaric oxygen preconditioning involves upregulation of hypoxia-inducible factor-1alpha and erythropoietin in rats.

@article{Gu2008MechanismOI,
  title={Mechanism of ischemic tolerance induced by hyperbaric oxygen preconditioning involves upregulation of hypoxia-inducible factor-1alpha and erythropoietin in rats.},
  author={Guojun Gu and Yun-ping Li and Zhang Peng and Jia-jun Xu and Zhi-min Kang and Weigang Xu and Heng-yi Tao and Robert P. Ostrowski and John H. Zhang and Xue-jun Sun},
  journal={Journal of applied physiology},
  year={2008},
  volume={104 4},
  pages={
          1185-91
        }
}
We studied the effect of hyperbaric oxygen (HBO) preconditioning on the molecular mechanisms of neuroprotection in a rat focal cerebral ischemic model. Seventy-two male Sprague-Dawley rats were pretreated with HBO (100% O(2), 2 atmospheres absolute, 1 h once every other day for 5 sessions) or with room air. In experiment 1, HBO-preconditioned rats and matched room air controls were subjected to focal cerebral ischemia or sham surgery. Postinjury motor parameters and infarction volumes of HBO… 
View on PubMed
image.sciencenet.cn
102 Citations
Highly Influential Citations
5
Background Citations
34
Methods Citations
6

Figures from this paper

102 Citations

Cyclo-Oxygenase-2 Mediates Hyperbaric Oxygen Preconditioning-Induced Neuroprotection in the Mouse Model of Surgical Brain Injury

HBO-PC attenuates postoperative brain edema and improves neurological outcomes after SBI, and the HBO-PC-induced neuroprotection is mediated through COX-2 signaling pathways.

Cyclooxygenase-2 Mediates Hyperbaric Oxygen Preconditioning in the Rat Model of Transient Global Cerebral Ischemia

HBO-PC increased the number of surviving neurons in the Cornu Ammonis area 1, which was associated with the reduced COX-2 expression in the hippocampus and in the cerebral cortex at 1 and 3 days after ischemia, thereby implicating COx-2 as a mediator of HBO-PC in the ischemic brain.

Hyperbaric oxygen preconditioning induces tolerance against brain ischemia–reperfusion injury by upregulation of antioxidant enzymes in rats

Up-regulated HIF-1α is involved in the hypoxic tolerance induced by hyperbaric oxygen preconditioning

Autophagy activation is involved in neuroprotection induced by hyperbaric oxygen preconditioning against focal cerebral ischemia in rats

SirT1 mediates hyperbaric oxygen preconditioning-induced ischemic tolerance in rat brain

  • Wenjun YanZongping Fang L. Xiong
  • Biology, Medicine
    Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
  • 2013
SirT1 mediates HBO-PC-induced tolerance to cerebral I/R through inhibition of apoptosis, which indicates that SirT1 is involved in neuroprotection elicited by HBO- PC in animal and cell culture models of ischemia.

Angiogenesis contributes to the neuroprotection induced by hyperbaric oxygen preconditioning against focal cerebral ischemia in rats

HBO-PC reduced brain injury and improved neurological function after focal cerebral ischemia, as partly mediated by the increased microvessel density in the penumbra, and this effect may result from the upregulation of Ang-2.

Hyperbaric oxygen preconditioning ameliorates hypoxia–ischemia brain damage by activating Nrf2 expression in vivo and in vitro

Observations demonstrated that an up-regulation of Nrf2 by HBO-PC might play an important role in the generation of tolerance against HIBD.

Hyperbaric Oxygen Preconditioning Protects Against Cerebral Ischemia/Reperfusion Injury by Inhibiting Mitochondrial Apoptosis and Energy Metabolism Disturbance

HBO-PC remarkably reduced the infarct volume and improved neurological deficits and inhibited the decrease in ATP levels, mitochondrial complex enzyme activities, and Na+/K+ ATPase activity to maintain stable energy metabolism.

Nrf2 activation in astrocytes contributes to spinal cord ischemic tolerance induced by hyperbaric oxygen preconditioning.

It is demonstrated that spinal cord ischemic tolerance induced by HBO-PC may be mainly related to Nrf2 activation in astrocytes, which is key proteins for intracellular glutathione synthesis and transit.
...

References

SHOWING 1-10 OF 53 REFERENCES

Heat Acclimation Increases Hypoxia-Inducible Factor 1α and Erythropoietin Receptor Expression: Implication for Neuroprotection after Closed Head Injury in Mice

The improved outcome of acclimated mice taken together with the basal and postinjury upregulation of the examined proteins suggests the involvement of this pathway in HA-induced neuroprotection.

Normobaric Hypoxia Induces Tolerance to Focal Permanent Cerebral Ischemia in Association with an Increased Expression of Hypoxia-Inducible Factor-1 and its Target Genes, Erythropoietin and VEGF, in the Adult Mouse Brain

The authors' findings show that hypoxia elicits a delayed, short-lasting (<72 hours) tolerance to focal permanent ischemia in the adult mouse brain, and this model might be a useful paradigm to further study the mechanisms of ischemic tolerance, to identify new therapeutic targets for stroke.

Hyperbaric oxygen preconditioning induces neuroprotection against ischemia in transient not permanent middle cerebral artery occlusion rat model.

It is demonstrated that HBO preconditioning can induce ischemic tolerance in transient not permanent MCAO rats in a "dose-dependent" manner.

Hyperbaric oxygenation pretreatment induces catalase and reduces infarct size in ischemic rat myocardium

HBO pretreatment was found to condition the heart and enhance enzymatic activity and gene expression of catalase, thereby significantly reducing infarct size after reperfusion, implying that HBO preconditioning may be developed as a new preventive measure for reperfusions injury in the heart.

Erythropoietin Is a Paracrine Mediator of Ischemic Tolerance in the Brain: Evidence from an In Vitro Model

The results establish EPO as an important paracrine neuroprotective mediator of ischemic preconditioning and provide evidence for the following signaling cascade: HIF-1 is activated rapidly by hypoxia in astrocytes and EPO activates the neuronal EPO receptor and, subsequently, JAK-2 and thereby PI3K.

Erythropoietin prevents neuronal apoptosis after cerebral ischemia and metabolic stress

  • A. SirénM. Fratelli P. Ghezzi
  • Biology, Medicine
    Proceedings of the National Academy of Sciences of the United States of America
  • 2001
Data suggest that inhibition of neuronal apoptosis underlies short latency protective effects of EPO after cerebral ischemia and other brain injuries, and the neurotrophic actions suggest there may be longer-latency effects as well.

HIF-1alpha-targeted pathways are activated by heat acclimation and contribute to acclimation-ischemic cross-tolerance in the heart.

It is concluded that HIF-1 contributes to the acclimation-ischemia cross-tolerance mechanism in the heart by induction of both chronic and inducible adaptive components.

Hyperbaric oxygenation induced tolerance against focal cerebral ischemia in mice is strain dependent

Hyperbaric oxygen reduces acetaminophen toxicity and increases HIF-1alpha expression.

Hyperbaric oxygen reduced early APAP-induced hepatocellular injury and HBO2 increases HIF-1alpha protein levels and DNA binding without a corresponding increase in transcriptional activity.

Cerebral ischemic preconditioning. An experimental phenomenon or a clinical important entity of stroke prevention?

The preconditioning mechanism induced is characterized by a brief episode of ischemia that renders the brain more resistant against subsequent longer ischemic events and provides the focus for further understanding of the mechanism of endogenous neuroprotection and the potential of novel therapeutic strategies for neuroprotection.
...