Ischaemia-reperfusion injury and hyperbaric oxygen pathways: a review of cellular mechanisms

Francis, Ashish; Baynosa, Richard C.

doi:10.28920/dhm47.2.110-117

Cited by 99 publications

(36 citation statements)

References 66 publications

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“…Due to multiple pathological mechanisms, cognitive impairments are usually the predominant symptoms localised in multiple brain areas (Kushner, 1998;Levin, 1990;Sohlberg & Mateer, 2001a, b). The use of HBOT for brain injury is based on the hypothesis that injured or inactive neurons would benefit from increased blood flow and oxygen delivery, which would act to metabolically or electrically reactivate the cells (Deng, 2018;Francis & Baynosa, 2017;Neubauer & James, 1998).…”

Section: Hbot and Tbi-related Cognition Disordersmentioning

confidence: 99%

Impact of Hyperbaric Oxygen Therapy on Cognitive Functions: a Systematic Review

et al. 2021

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Hyperbaric oxygen therapy (HBOT) is a modality of treatment in which patients inhale 100% oxygen inside a hyperbaric chamber pressurised to greater than 1 atmosphere. The aim of this review is to discuss neuropsychological findings in various neurological disorders treated with HBOT and to open new perspectives for therapeutic improvement. A literature search was conducted in the MEDLINE (via PubMed) database from the inception up 10 May 2020. Eligibility criteria included original articles published in English. Case studies were excluded. Full-text articles were obtained from the selected studies and were reviewed on the following inclusion criteria (1) performed cognitive processes assessment (2) performed HBOT with described protocol. Two neuropsychologists independently reviewed titles, abstracts, full texts and extracted data. The initial search retrieved 1024 articles, and a total of 42 studies were finally included after applying inclusion and exclusion criteria. The search yielded controversial results with regard to the efficiency of HBOT in various neurological conditions with cognitive disturbance outcome. To the best of our knowledge this is the first state-of-the art, systematic review in the field. More objective and precise neuropsychological assessment methods are needed to exact evaluation of the efficacy of HBOT for neuropsychological deficits. Future studies should widen the assessment of HBOT effects on different cognitive domains because most of the existing studies have focussed on a single process. Finally, there is a need for further longitudinal studies.

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Section: Hbot and Tbi-related Cognition Disordersmentioning

confidence: 99%

Impact of Hyperbaric Oxygen Therapy on Cognitive Functions: a Systematic Review

et al. 2021

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“…This therapeutic modality is based upon administration of 100% molecular oxygen under the increased pressure, most frequently two times greater than the atmospheric pressure at sea level [ 8 ]. HBO preconditioning and therapy provide protective and beneficial effects in I/R injury, especially of brain and heart [ 9 , 10 , 11 ]. On the other hand, there are not much data about the effects of HBO preconditioning applied in experimental models of postischemic AKI, especially accompanied with hypertension [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

Hyperbaric Oxygen Preconditioning Upregulates Heme OxyGenase-1 and Anti-Apoptotic Bcl-2 Protein Expression in Spontaneously Hypertensive Rats with Induced Postischemic Acute Kidney Injury

Ostojic

Ivanov

Mihailović-Stanojević

et al. 2021

IJMS

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Renal ischemia and reperfusion (I/R) injury is the most common cause of acute kidney injury (AKI). Pathogenesis of postischemic AKI involves hemodynamic changes, oxidative stress, inflammation process, calcium ion overloading, apoptosis and necrosis. Up to date, therapeutic approaches to treat AKI are extremely limited. Thus, the aim of this study was to evaluate the effects of hyperbaric oxygen (HBO) preconditioning on citoprotective enzyme, heme oxygenase-1 (HO-1), pro-apoptotic Bax and anti-apoptotic Bcl-2 proteins expression, in postischemic AKI induced in normotensive Wistar and spontaneously hypertensive rats (SHR). The animals were randomly divided into six experimental groups: SHAM-operated Wistar rats (W-SHAM), Wistar rats with induced postischemic AKI (W-AKI) and Wistar group with HBO preconditioning before AKI induction (W-AKI + HBO). On the other hand, SHR rats were also divided into same three groups: SHR-SHAM, SHR-AKI and SHR-AKI + HBO. We demonstrated that HBO preconditioning upregulated HO-1 and anti-apoptotic Bcl-2 protein expression, in both Wistar and SH rats. In addition, HBO preconditioning improved glomerular filtration rate, supporting by significant increase in creatinine, urea and phosphate clearances in both rat strains. Considering our results, we can also say that even in hypertensive conditions, we can expect protective effects of HBO preconditioning in experimental model of AKI.

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“…Necrotic regions and a large number of apoptotic cells were observed in the brains of these fish through transmission electron microscopy. These observations indicate that return to normal temperature at 28 °C (rewarming) augmented the tissue damages, which resembles the phenomenon of ischemia–reperfusion injury [ 45 ]. It is likely that the metabolic burden accumulated during cold exposure was released upon rewarming thus led to extensive molecular damages and cell death.…”

Section: Discussionmentioning

confidence: 99%

Characterization of Biological Pathways Regulating Acute Cold Resistance of Zebrafish

Ren

Long

Liu

et al. 2021

IJMS

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Low temperature stress represents a major threat to the lives of both farmed and wild fish species. However, biological pathways determining the development of cold resistance in fish remain largely unknown. Zebrafish larvae at 96 hpf were exposed to lethal cold stress (10 °C) for different time periods to evaluate the adverse effects at organism, tissue and cell levels. Time series RNA sequencing (RNA-seq) experiments were performed to delineate the transcriptomic landscape of zebrafish larvae under cold stress and during the subsequent rewarming phase. The genes regulated by cold stress were characterized by progressively enhanced or decreased expression, whereas the genes associated with rewarming were characterized by rapid upregulation upon return to normal temperature (28 °C). Genes such as trib3, dusp5 and otud1 were identified as the representative molecular markers of cold-induced damages through network analysis. Biological pathways involved in cold stress responses were mined from the transcriptomic data and their functions in regulating cold resistance were validated using specific inhibitors. The autophagy, FoxO and MAPK (mitogen-activated protein kinase) signaling pathways were revealed to be survival pathways for enhancing cold resistance, while apoptosis and necroptosis were the death pathways responsible for cold-induced mortality. Functional mechanisms of the survival-enhancing factors Foxo1, ERK (extracellular signal-regulated kinase) and p38 MAPK were further characterized by inhibiting their activities upon cold stress and analyzing gene expression though RNA-seq. These factors were demonstrated to determine the cold resistance of zebrafish through regulating apoptosis and p53 signaling pathway. These findings have provided novel insights into the stress responses elicited by lethal cold and shed new light on the molecular mechanisms underlying cold resistance of fish.

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Ischaemia-reperfusion injury and hyperbaric oxygen pathways: a review of cellular mechanisms

Cited by 99 publications

References 66 publications

Impact of Hyperbaric Oxygen Therapy on Cognitive Functions: a Systematic Review

Impact of Hyperbaric Oxygen Therapy on Cognitive Functions: a Systematic Review

Hyperbaric Oxygen Preconditioning Upregulates Heme OxyGenase-1 and Anti-Apoptotic Bcl-2 Protein Expression in Spontaneously Hypertensive Rats with Induced Postischemic Acute Kidney Injury

Characterization of Biological Pathways Regulating Acute Cold Resistance of Zebrafish

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