The protection effect and mechanism of hyperbaric oxygen therapy in rat brain with traumatic injury

Xing, Pengcheng; Ma, Ke; Li, Lijuan; Wang, Donglian; Hu, Guoyong; Wei, Long

doi:10.1590/s0102-865020180040000006

Cited by 18 publications

(9 citation statements)

References 42 publications

(39 reference statements)

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“…This result proved that HBO therapy suppressed caspase 3 activity and attenuated the neuronal apoptosis induced by acute TBI. It is consistent with previous studies 28,29…”

Section: Discussionsupporting

confidence: 94%

<p>Hyperbaric oxygen therapy attenuates neuronal apoptosis induced by traumatic brain injury via Akt/GSK3β/β-catenin pathway</p>

He³

2019

NDT

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BackgroundGiven that the therapeutic effect of hyperbaric oxygen (HBO) therapy on traumatic brain injury (TBI) has been debated for a long time, it is necessary to clarify the mechanism underlying the effect of HBO on acute TBI.MethodsThis study investigated the effect of HBO therapy on neuronal apoptosis induced by acute TBI using the mouse model of TBI. The number of apoptotic cells and expression of apoptosis-associated factors (including caspase 3, pAkt/Akt, pGSK3β/GSK3β, and β-catenin) in pericontusional cortices of mice exposed to sham, TBI, and TBI + HBO treatment were measured and analyzed using TUNEL assay, quantitative reverse-transcription PCR, and Western blot.ResultsResults showed that acute TBI increased the number of apoptotic neurons and mRNA expression and activated caspase 3 protein. With regard to proteins, acute TBI also resulted in decreased levels of pAkt/Akt, pGSK3β/GSK3β, and β-catenin, which facilitates neuronal apoptosis. This study shows that HBO therapy reversed these changes of pAkt/Akt, pGSK3β/ GSK3β, and β-catenin induced by acute TBI and attenuated the apoptotic process in the pericontusional cortex.ConclusionThis study demonstrates the beneficial effect of HBO therapy on neuronal apoptosis caused by acute TBI. Furthermore, the mechanism underlying the therapeutic effect of HBO on acute TBI partly involves the Akt/GSK3β/β-catenin pathway.

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“…This result proved that HBO therapy suppressed caspase 3 activity and attenuated the neuronal apoptosis induced by acute TBI. It is consistent with previous studies 28,29…”

Section: Discussionsupporting

confidence: 94%

<p>Hyperbaric oxygen therapy attenuates neuronal apoptosis induced by traumatic brain injury via Akt/GSK3β/β-catenin pathway</p>

He³

2019

NDT

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“…In the end, testing a variety of HBOT conditions in clinically relevant models are critical to achieving the optimal safe and effective regimen of mitochondria transfer‐mediated neuroprotection . Recent studies have established successful protocols for testing HBOT in rodent models for both single and multiple treatments . Due to prior FDA‐approved indications, HBOT has an established infrastructure in clinics allowing for it to be quickly implemented once treatments are optimized for humans …”

Section: Discussionmentioning

confidence: 99%

“…52 Recent studies have established successful protocols for testing HBOT in rodent models for both single and multiple treatments. 53 Due to prior FDA-approved indications, HBOT has an established infrastructure in clinics allowing for it to be quickly implemented once treatments are optimized for humans. 19,20 HBOT preconditioning poses as a prophylactic treatment for sequestration of inflammation, which is a pathological condition rampant in many cerebrovascular diseases.…”

Section: Discussionmentioning

confidence: 99%

Prophylactic treatment of hyperbaric oxygen treatment mitigates inflammatory response via mitochondria transfer

Lippert

Borlongan²

2019

CNS Neurosci Ther

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Summary Aims Hyperbaric oxygen therapy (HBOT) has been widely used as postinjury treatment; however, we investigate its ability to mitigate potential damage as a preconditioning option. Here, we tested the hypothesis that HBOT preconditioning mitigates cell death in primary rat neuronal cells (PRNCs) through the transfer of mitochondria from astrocytes. Methods Primary rat neuronal cells were subjected to a 90‐minute HBOT treatment at 2.5 absolute atmospheres prior to either tumor necrosis factor‐alpha (TNF‐alpha) or lipopolysaccharide (LPS) injury to simulate the inflammation‐plagued secondary cell death associated with stroke and traumatic brain injury (TBI). After incubation with TNF‐alpha or LPS, the cell viability of each group was examined. Results There was a significant increase of cell viability accompanied by mitochondrial transfer in the injury groups that received HBOT preconditioning compared to the injury alone groups (44 ± 5.2 vs 68 ± 4.48, n = 20, P < 0.05). The transfer of mitochondria directly after HBOT treatment was visualized by capturing images in 5‐minute intervals, which revealed that the robust transfer of mitochondria begins soon after HBOT and persisted throughout the treatment. Conclusion This study shows that HBOT preconditioning stands as a robust prophylactic treatment for sequestration of inflammation inherent in stroke and TBI, possibly facilitating the transfer of resilient mitochondria from astrocytes to inflammation‐susceptible neuronal cells in mitigating cell death.

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“…[52] Recent studies have been able to test HBOT treatments on rodent models allowing them to find successful protocols. [53]…”

Section: Applying Hyperbaric Oxygen Therapy To Clinicsmentioning

confidence: 99%

Hyperbaric oxygen therapy: A new look on treating stroke and traumatic brain injury

et al. 2019

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Although hyperbaric oxygen therapy (HBOT) is common as a treatment for injuries, this study aimed to research the ability of HBOT in preconditioning to diminish any potential damage. The hypothesis stated that HBOT preconditioning alleviated the death of cells in primary rat neuronal cells (PRNCs) by transferring mitochondria from astrocytes. In this experiment, PRNCs were given an HBOT treatment before a tumor necrosis factor-alpha or lipopolysaccharide injury which resembled cell death associated with stroke and traumatic brain injury (TBI). After being examined, the study found more cell viability in the PRNCs that had received HBOT precondition and a mitochondrial transfer. The mitochondrial transfer was visualized by a series of images showing the transfer after the HBOT treatment. This study demonstrated the ability of HBOT preconditioning as a treatment for inflammation in stroke and TBI, with the transfer of mitochondria from astrocytes to PRNCs reducing cell death. Along with discussion of the study, this review also focuses on different stroke treatments in comparison with HBOT.

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The protection effect and mechanism of hyperbaric oxygen therapy in rat brain with traumatic injury

Abstract: Our findings provided evidence for the clinical usage of HBO treating brain damages.

Cited by 18 publications

References 42 publications

<p>Hyperbaric oxygen therapy attenuates neuronal apoptosis induced by traumatic brain injury via Akt/GSK3β/β-catenin pathway</p>

<p>Hyperbaric oxygen therapy attenuates neuronal apoptosis induced by traumatic brain injury via Akt/GSK3β/β-catenin pathway</p>

Prophylactic treatment of hyperbaric oxygen treatment mitigates inflammatory response via mitochondria transfer

Hyperbaric oxygen therapy: A new look on treating stroke and traumatic brain injury

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The protection effect and mechanism of hyperbaric oxygen therapy in rat brain with traumatic injury

Abstract: Our findings provided evidence for the clinical usage of HBO treating brain damages.

Cited by 18 publications

References 42 publications

<p>Hyperbaric oxygen therapy attenuates neuronal apoptosis induced by traumatic brain injury via Akt/GSK3&beta;/&beta;-catenin pathway</p>

<p>Hyperbaric oxygen therapy attenuates neuronal apoptosis induced by traumatic brain injury via Akt/GSK3&beta;/&beta;-catenin pathway</p>

Prophylactic treatment of hyperbaric oxygen treatment mitigates inflammatory response via mitochondria transfer

Hyperbaric oxygen therapy: A new look on treating stroke and traumatic brain injury

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<p>Hyperbaric oxygen therapy attenuates neuronal apoptosis induced by traumatic brain injury via Akt/GSK3β/β-catenin pathway</p>

<p>Hyperbaric oxygen therapy attenuates neuronal apoptosis induced by traumatic brain injury via Akt/GSK3β/β-catenin pathway</p>