Hyperbaric Oxygen Therapy in Acute Ischemic Stroke: A Review

Ding, Zheng; Tong, Wesley C.; Lu, Xiyi; Peng, Huiping

doi:10.1159/000362677

Cited by 52 publications

(43 citation statements)

References 92 publications

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“…HBO treatment for 2 days or 3 weeks decreases expression of MPO, with the longer course treatment more effective in reducing MPO levels (Lee et al, 2013). HBO also suppresses leukocyte accumulation in the brain ischemic area and inhibits neutrophil–endothelial interactions caused by ischemia/reperfusion injury (Buras and Reenstra, 2007; Ding et al, 2014). …”

Section: Recently Identified Therapeutic Aims and Therapiesmentioning

confidence: 99%

Targeting vascular inflammation in ischemic stroke: Recent developments on novel immunomodulatory approaches

Shekhar

Cunningham

Pabbidi

et al. 2018

European Journal of Pharmacology

100

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Ischemic stroke is a devastating and debilitating medical condition with limited therapeutic options. However, accumulating evidence indicates a central role of inflammation in all aspects of stroke including its initiation, the progression of injury, and recovery or wound healing. A central target of inflammation is disruption of the blood brain barrier or neurovascular unit. Here we discuss recent developments in identifying potential molecular targets and immunomodulatory approaches to preserve or protect barrier function and limit infarct damage and functional impairment. These include blocking harmful inflammatory signaling in endothelial cells, microglia/macrophages, or Th17/γδ T cells with biologics, third generation epoxyeicosatrienoic acid (EET) analogs with extended half-life, and miRNA antagomirs. Complementary beneficial pathways may be enhanced by miRNA mimetics or hyperbaric oxygenation. These immunomodulatory approaches could be used to greatly expand the therapeutic window for thrombolytic treatment with tissue plasminogen activator (t-PA). Moreover, nanoparticle technology allows for the selective targeting of endothelial cells for delivery of DNA/RNA oligonucleotides and neuroprotective drugs. In addition, although likely detrimental to the progression of ischemic stroke by inducing inflammation, oxidative stress, and neuronal cell death, 20-HETE may also reduce susceptibility of onset of ischemic stroke by maintaining autoregulation of cerebral blood flow. Although the interaction between inflammation and stroke is multifaceted, a better understanding of the mechanisms behind the pro-inflammatory state at all stages will hopefully help in developing novel immunomodulatory approaches to improve mortality and functional outcome of those inflicted with ischemic stroke.

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Section: Recently Identified Therapeutic Aims and Therapiesmentioning

confidence: 99%

Targeting vascular inflammation in ischemic stroke: Recent developments on novel immunomodulatory approaches

Shekhar

Cunningham

Pabbidi

et al. 2018

European Journal of Pharmacology

100

View full text Add to dashboard Cite

show abstract

“…Stroke, known as cerebrovascular disease, is a common and devastating neurological disease, which is characterized by high mortality and morbidity rates [1]. Ischemic stroke, accounts for 80% of stroke, which is mainly caused by an insufficient supply of glucose and oxygen to central nervous system (CNS) tissue and thus resulting in a significant amount of cell damages [2].…”

Section: Introductionmentioning

confidence: 99%

Maternally Expressed Gene 3 (MEG3) Enhances PC12 Cell Hypoxia Injury by Targeting MiR-147

Han

Dong

Liu

et al. 2017

Cell Physiol Biochem

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Background/Aims: Cerebral ischemia often leads to breakdown of blood–brain barrier (BBB) and vasogenic edema. It remains to be established whether MEG3 is responsible for the hypoxic damage in neural cells. This study aimed to investigate the role of MEG3 in the hypoxia-induced injuries of PC12 cells. Methods: The PC12 cells were seeded and cultured under hypoxia and normoxia culture conditions. The cell viability determined by trypan blue exclusion, apoptosis using propidium iodide (PI) and fluorescein isothiocynate (FITC)-conjugated Annexin V staining, cell-migration using a modified two-chamber migration assay with a pore size of 8 µM and invasion using 24-well Millicell Hanging Cell Culture inserts with 8 µM PET membranes. Results: Cell viability, relative migration and relative invasion decreased significantly in PC12 cells injured due to hypoxia as compared to control cells. An increase in apoptosis was also observed. The expression of MEG3 was up-regulated in hypoxia-injured PC12 cells. MEG3 overexpression enhanced hypoxia injuries, while MEG3 suppression attenuated the injuries. Meanwhile, MEG3 negatively regulated miR-147 expression. In addition, we found that the expression of Sox2 was increased in PC12 cells after hypoxia and miR-147 negatively regulated Sox2 expression through targets its 3’-UTR. Interesting, Sox2 activated NF-κB pathway and Wnt/β-catenin pathway in PC12 cells. Conclusion: Considering the observations in our study, we can conclude that MEG3 aggravated the hypoxial injury in PC12 cells by down-regulating miR-147 gene and miR-147 further negatively regulated Sox2 expression.

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“…Recent animal studies suggest that hyperbaric oxygen therapy has several beneficial mechanisms in acute ischaemic stroke12 perhaps specifically helping to modulate secondary injury after reperfusion 13 14. However, its benefit in humans remains uncertain unless there is a cerebral arterial gas embolism 15…”

Section: Discussionmentioning

confidence: 99%

Cerebral arterial gas embolism from attempted mechanical thrombectomy: recovery following hyperbaric oxygen therapy

et al. 2017

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Cerebral arterial gas embolism is a recognised complication of endovascular intervention with an estimated incidence of 0.08%. Its diagnosis is predominantly clinical, supported by neuroimaging. The treatment relies on alleviating mechanical obstruction and reversing the proinflammatory processes that contribute to tissue ischaemia. Hyperbaric oxygen therapy is an effective treatment and has multiple mechanisms to reverse the pathological processes involved in cerebral arterial gas embolism. Symptomatic cerebral arterial gas embolism is a rare complication of endovascular intervention for acute ischaemic stroke. Although there are no previous descriptions of its successful treatment with hyperbaric oxygen therapy following mechanical thrombectomy, this is likely to become more common as mechanical thrombectomy is increasingly used worldwide to treat acute ischaemic stroke.

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Hyperbaric Oxygen Therapy in Acute Ischemic Stroke: A Review

Cited by 52 publications

References 92 publications

Targeting vascular inflammation in ischemic stroke: Recent developments on novel immunomodulatory approaches

Targeting vascular inflammation in ischemic stroke: Recent developments on novel immunomodulatory approaches

Maternally Expressed Gene 3 (MEG3) Enhances PC12 Cell Hypoxia Injury by Targeting MiR-147

Cerebral arterial gas embolism from attempted mechanical thrombectomy: recovery following hyperbaric oxygen therapy

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