Outcome

In conclusion this study demonstrates the significant protective effects of hyperbaric oxygen therapy (HBOT) as a preconditioning treatment for stroke and traumatic brain injury (TBI). By administering a single 90-minute HBOT session at 2.5 absolute atmospheres (ATA) before injury researchers observed a notable increase in cell viability—68% compared to 44% in non-treated groups.

Introduction

Hyperbaric oxygen therapy (HBOT) performed at 2.5 ATA for 90 minutes before injury increased cell viability from 44% to 68% in neuronal cells exposed to inflammation. This improvement was likely due to the early and persistent transfer of mitochondria from astrocytes to neurons suggesting HBOT preconditioning as a promising strategy to reduce inflammation-induced cell death in stroke and traumatic brain injury.

Results

Administering a single 90-minute session of Hyperbaric Oxygen Therapy (HBOT) at 2.5 atmospheres absolute (ATA) before injury significantly improved cell viability in neuronal cells exposed to inflammation. In the HBOT preconditioned group cell viability was increased to 68% compared to 44% in the non-treated injury group. This notable enhancement in cell viability is attributed to the early and persistent transfer of resilient mitochondria from astrocytes to neuronal cells as observed through live imaging. The mitochondrial transfer began shortly after the HBOT session and continued throughout the treatment period. These findings underline HBOT preconditioning as a potent intervention to mitigate inflammation-induced cell death particularly in conditions such as stroke and traumatic brain injury (TBI). By facilitating the transfer of mitochondria HBOT enhances the intrinsic cellular resilience thereby offering a promising strategy to reduce neuroinflammation and subsequent neuronal damage.

Conclusion

In conclusion this study highlights the significant protective effects of hyperbaric oxygen therapy (HBOT) as a preconditioning treatment for mitigating brain damage associated with stroke and traumatic brain injury (TBI). Administering a single 90-minute HBOT session at 2.5 atmospheres absolute (ATA) before injury led to a marked increase in cell viability from 44% in untreated groups to 68% in HBOT preconditioned groups. The observed improvement is likely due to the early and sustained transfer of resilient mitochondria from astrocytes to neuronal cells which helps reduce inflammation-induced cell death.

These findings underscore HBOT preconditioning as a promising prophylactic strategy to enhance cell survival and reduce neurological damage in stroke and TBI. The potential of this treatment to improve clinical outcomes merits further investigation particularly in human trials to establish its efficacy and safety across broader patient populations. Future research should also explore the molecular mechanisms underpinning mitochondrial transfer and resilience aiming to optimize HBOT protocols for maximum therapeutic benefit.