Outcome

This study reveals that hyperbaric oxygen therapy (HBOT) at 2.4 atmospheres significantly regulates over 8100 genes in human microvascular endothelial cells (HMEC-1). Key genes such as immediate early transcription factors (FOS FOSB JUNB) and metallothioneins exhibited notable responses both immediately and 24 hours post-treatment. The research underscores the role of the Nrf-2 oxidative stress response pathway in cellular defense and proliferation highlighting that HBOT enhances these processes more effectively than 100% oxygen at normal pressure.

Introduction

Hyperbaric oxygen therapy (HBOT) at 2.4 atmospheres absolute (ATA) has been demonstrated to significantly impact gene expression in human microvascular endothelial cells (HMEC-1). This study identified that a single 60-minute HBOT session modulates the expression of over 8100 genes affecting key elements such as immediate early transcription factors (FOS FOSB JUNB) metallothioneins and molecular chaperones involved in oxidative stress response and cellular protection. Notably the Nrf-2 oxidative stress response pathway was markedly activated facilitating enhanced cell proliferation and defense mechanisms more effectively than 100% oxygen at normal pressure. Furthermore two daily HBOT treatments proved to enhance vascular tube formation more strongly than a single session highlighting the potential of HBOT to promote wound healing and angiogenesis. These findings suggest that incorporating HBOT in therapeutic protocols could significantly benefit wound healing processes and preconditioning patients before major surgeries to better protect and repair endothelial cells.

Results

Hyperbaric oxygen therapy (HBOT) at 2.4 atmospheres absolute (ATA) significantly impacted gene expression in human microvascular endothelial cells (HMEC-1). A single 60-minute session resulted in the regulation of over 8100 genes with changes detectable immediately and up to 24 hours post-treatment. Notable among the affected genes were immediate early transcription factors (such as FOS FOSB JUNB) and metallothioneins which are involved in metal metabolism and detoxification.

The study highlighted the substantial impact of HBOT on the Nrf-2 mediated oxidative stress response pathway. The activation of this pathway suggests that HBOT enhances cellular defenses against oxidative stress outperforming the effect of 100% oxygen at normal pressure. This increase in cellular defense was accompanied by improved cell proliferation and repair.

Cellular functions such as the cell cycle movement morphology gene expression and growth were influenced by HBOT. The therapy’s ability to protect cells from oxidative damage and support cell proliferation was particularly notable. The results indicate that HBOT may be more effective than oxygen therapy alone in fostering these beneficial changes.

In addition to the genetic and cellular modifications the study demonstrated that HBOT significantly promoted vascular tube formation in HMEC-1 cells. Two daily HBOT sessions enhanced tube formation more efficiently than a single session underscoring HBOT’s potential to stimulate angiogenesis and improve endothelial repair. This aspect is particularly relevant for enhancing wound-healing protocols and preconditioning patients before major surgeries to boost cellular protection and repair mechanisms.

In summary the study delineates the significant molecular and cellular responses elicited by HBOT in endothelial cells highlighting its potential to improve therapeutic outcomes in wound healing and surgical preconditioning by leveraging enhanced oxidative stress defense and vascular formation capabilities.

Conclusion

In conclusion this study provides valuable insights into the molecular impact of hyperbaric oxygen therapy (HBOT) on human microvascular endothelial cells (HMEC-1) at 2.4 atmospheres absolute (ATA) with 100% oxygen. The key findings reveal significant regulation of over 8100 genes following a single 60-minute HBOT session including the prominent response of immediate early transcription factors (FOS FOSB JUNB) and metallothioneins. Notably the Nrf-2 mediated oxidative stress response pathway was significantly activated enhancing cellular protection against oxidative stress and promoting cell proliferation more effectively than 100% oxygen at normal pressure.

The study also demonstrated that administering two daily HBOT sessions markedly improved vascular tube formation highlighting its potential to enhance angiogenesis and endothelial cell repair. These findings underscore the importance of elevated pressure in HBOT to achieve substantial biological responses beyond what is achieved with 100% oxygen alone.

The implications of this research are significant for refining HBOT protocols particularly for wound healing and preconditioning patients before major surgeries. Future research could further explore the detailed mechanisms and long-term effects of HBOT on gene expression and cellular functions paving the way for broader clinical applications to improve patient outcomes in conditions involving vascular and endothelial dysfunctions.