The acute antinociceptive effect of hyperbaric oxygen is not accompanied by an increase in markers of oxidative stress

Liu, Shulin; Shirachi, Donald Y.; Quock, Raymond M.

doi:10.1016/j.lfs.2013.12.207

Cited by 9 publications

(10 citation statements)

References 29 publications

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“…In physiological conditions, reactive oxygen species (ROS) are subproducts of oxidative phosphorylation inside the mitochondria (Taniyama and Griendling, ; Liu et al, ; Zhou et al, ; Rönn et al, ). However, in inflammatory conditions, activated macrophages secrete metalloproteinases that increases ROS concentration and the intracellular oxidative stress promoted by this situation can blockade eNOS activity (Vaddi et al, ).…”

Section: Resultsmentioning

confidence: 99%

Hyperbaric oxygen affects endothelial progenitor cells proliferation in vitro

Benincasa

Filho

Carneiro

et al. 2019

Cell Biology International

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Hyperbaric oxygen is a clinical treatment that contributes to wound healing by increasing fibroblasts proliferation, collagen synthesis, and production of growth factors, inducing angiogenesis and inhibiting antimicrobial activity. It also has been shown that hyperbaric oxygen treatment (HBO), through the activation of nitric oxide synthase promotes an increase in the nitric oxide levels that may improve endothelial progenitor cells (EPC) mobilization from bone marrow to the peripheral blood and stimulates the vessel healing process. However, cellular mechanisms involved in cell proliferation and activation of EPC after HBO treatment remain unknown. Therefore, the present work aimed to analyze the effect of HBO on the proliferation of pre-treated bone marrow-derived EPC with TNF-alpha. Also, we investigated the expression of ICAM and eNOS by immunochemistry, the production of reactive species of oxygen and performed an in vitro wound healing. Although 1h of HBO treatment did not alter the rate of in vitro wound closure or cell proliferation, it increased eNOS expression and decreased ICAM expression and reactive oxygen species production in cells pre-treated with TNF-alpha. These results indicate that HBO can decrease the inflammatory response in endothelial cells mediated by TNF-alpha, and thus, promote vascular recovery after injury.Additional supporting information may be found online in the Supporting Information section at the end of the article. Figure S1. Effect of 100% oxygen on ICAM expression.HBO affects activated EPC proliferation J. C. Benincasa et al.

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Section: Resultsmentioning

confidence: 99%

Hyperbaric oxygen affects endothelial progenitor cells proliferation in vitro

Benincasa

Filho

Carneiro

et al. 2019

Cell Biology International

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“…Preliminary experiments demonstrated that neither 100% O 2 nor 3.5 ATA alone produced any antinociceptive effect; only the combination of 100% O 2 and 3.5 ATA evoked an antinociceptive response (Liu et al, 2013; Liu et al, unpublished manuscript under review).…”

Section: Methodsmentioning

confidence: 99%

Involvement of brain opioid receptors in the anti-allodynic effect of hyperbaric oxygen in rats with sciatic nerve crush-induced neuropathic pain

et al. 2013

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Earlier research has demonstrated that hyperbaric oxygen (HBO2) can produce an antinociceptive effect in models of acute pain. Recent studies have revealed that HBO2 can produce pain relief in animal models of chronic pain as well. The purpose of the present investigation was to ascertain whether HBO2 treatment might suppress allodynia in rats with neuropathic pain and whether this effect might be blocked by the opioid antagonist naltrexone (NTX). Male Sprague Dawley rats were subjected to a sciatic nerve crush under anesthesia and mechanical thresholds were assessed using an electronic von Frey anesthesiometer. The time course of the HBO2-induced anti-allodynic effect in different treatment groups was plotted, and the area-under-the-curve (AUC) was determined for each group. Seven days after the nerve crush procedure, rats were treated with HBO2 at 3.5 atmospheres absolute (ATA) for 60 min and exhibited an anti-allodynic effect, compared to nerve crush-only control rats. Twenty-four hours before HBO2 treatment, another group of rats was implanted with Alzet® osmotic minipumps that continuously released NTX into the lateral cerebral ventricle for 7 days. These NTX-infused, HBO2-treated rats exhibited an allodynic response comparable to that exhibited by rats receiving nerve crush only. Analysis of the AUC data showed that HBO2 significantly reduced the nerve crush-induced allodynia; this anti-allodynic effect of HBO2 was reversed by NTX. These results implicate opioid receptors in the pain relief induced by HBO2.

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“…HBOT has been shown to promote neuronal survival, decrease the apoptosis of brain injury via a reduction in oxidative stress to modulate neuroinflammation. (Liu et al, 2014 ). Our results showed that HBO intervention could downregulate the expression of histones H1, H2A, H4 induced by TBI, while the decline in 1.6ATA groups was significantly lower than that in the 2.2ATA group, especially within 6 h. It confirmed preliminarily that 1.6ATA HBO might reduce secondary damage of TBI through inhibiting histone release more efficiently than 2.2ATA HBO.…”

Section: Discussionmentioning

confidence: 99%

The effect of different atmosphere absolute hyperbaric oxygen on the expression of extracellular histones after traumatic brain injury in rats

Liang

Sun

Yang

et al. 2020

Cell Stress and Chaperones

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By observing the dynamic changes of extracellular histones H1, H2A, H4, and NF-κB expression in brain tissues after brain injury in rats, we explore the association among the expression of extracellular histones H1, H2A, H4, and NF-κB following traumatic brain injury (TBI), as well as the effect of different atmospheres absolute hyperbaric oxygen (HBO) intervention on the expression and possible mechanisms. A total of 120 SD rats were randomly divided into 4 groups: Sham-operated (SH), TBI (traumatic brain injury) group, traumatic brain injury and hyperbaric oxygen treatment 1.6ATA (TBI + HBO1) group, and traumatic brain injury and hyperbaric oxygen treatment2.2ATA (TBI + HBO2) group, with 30 rats in each group. The rats in each group were then randomly divided into five smaller time-specific sub-groups: 3 h, 6 h, 12 h, 24 h, and 48 h after surgery. TBI models were established, and the brain tissue around the lesion was taken at different time points. On the one hand,we detected the level of local histones H1, H2A, H4, and NF-κB by RT-PCR and Western Blot. On the other hand, we used immunohistochemical methods to detect the expression of NF-κB, while using the TUNEL method to observe the cell apoptosis in experimental groups after brain injury. Extracellular histones H1, H2A, H4, and NF-κB proteins were highly expressed at 3 h, then with a slight fluctuation, reached to peak at 48 h after the injury. HBO can affect the expression of histones H1, H2A, H4, and NF-κB. The decline of each indicator in the 1.6ATA group was significantly lower than that in the 2.2ATA group, especially within 6 h (P < 0. 05). In addition, NF-κB expression was consistent with the pathological changes of apoptosis in experimental groups. Hyperbaric oxygen therapy with relatively low pressure (1.6ATA) at the early stage can significantly inhibit the expression of extracellular histones H1, H2A, H4, and NF-κB around the lesion, reduce the apoptosis of nerve cells, and thus play an important role in alleviating secondary brain injury.

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The acute antinociceptive effect of hyperbaric oxygen is not accompanied by an increase in markers of oxidative stress

Cited by 9 publications

References 29 publications

Hyperbaric oxygen affects endothelial progenitor cells proliferation in vitro

Hyperbaric oxygen affects endothelial progenitor cells proliferation in vitro

Involvement of brain opioid receptors in the anti-allodynic effect of hyperbaric oxygen in rats with sciatic nerve crush-induced neuropathic pain

The effect of different atmosphere absolute hyperbaric oxygen on the expression of extracellular histones after traumatic brain injury in rats

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