Outcome

Hyperbaric oxygen therapy (HBOT) administered daily at 100% oxygen and 2.0 ATA for 60 minutes significantly reduced the onset of autoimmune diabetes in nonobese diabetic (NOD) mice. Cyclophosphamide-induced diabetes onset dropped from 85.3% in controls to 48% with HBOT while spontaneous diabetes incidence fell from 85% to 65%.

Introduction

Hyperbaric oxygen therapy (HBOT) has shown substantial promise as a therapeutic intervention in the context of autoimmune diabetes prevention. This study investigated the effects of HBOT administered daily at 100% oxygen and 2.0 atmospheres absolute (ATA) for 60 minutes on nonobese diabetic (NOD) mice. The results were notable: cyclophosphamide-induced diabetes onset was reduced from 85.3% in control mice to 48% in the HBOT-treated group while spontaneous diabetes incidence decreased from 85% to 65%. Key immunological improvements were observed including lower insulitis scores reduced T-cell proliferation increased T-cell CD62L expression diminished costimulation markers and decreased dendritic cell MHC class II expression. Additionally HBOT significantly impacted β-cell dynamics reducing apoptosis and enhancing the proliferation of insulin-positive cells. These findings suggest that HBOT not only modulates immune responses but also preserves pancreatic β-cell function highlighting its potential as a noninvasive adjuvant therapy for the prevention of type 1 diabetes.

Results

The results of this study demonstrate that hyperbaric oxygen therapy (HBOT) administered daily at 100% oxygen and 2.0 atmospheres absolute (ATA) for 60 minutes significantly mitigates the onset of autoimmune diabetes in nonobese diabetic (NOD) mice. Specifically the incidence of diabetes triggered by cyclophosphamide was reduced from 85.3% in the control group to 48% with HBOT (P < 0.005). Additionally the incidence of spontaneous diabetes dropped from 85% to 65% in the HBOT-treated group (P = 0.01).

Further immunological analysis revealed that HBOT-treated prediabetic mice exhibited lower insulitis scores and a reduction in T-cell proliferation when stimulated in vitro (P < 0.03). Enhanced T-cell function was noted with increased expression of CD62L (P < 0.04) and a decrease in costimulation markers such as CD40 DC80 and CD86. There was also a significant reduction in MHC class II expression in dendritic cells (P < 0.025) indicating a lowered activation state of these antigen-presenting cells.

Moreover HBOT treatment resulted in a marked reduction in apoptosis (P < 0.01) and a notable increase in the proliferation of insulin-positive cells (P < 0.001). This suggests that HBOT not only modulates immune responses to mitigate autoimmune attacks but also helps in preserving and possibly enhancing β-cell mass by decreasing cell death and promoting cell proliferation.

These findings collectively suggest that HBOT can effectively reduce the incidence of autoimmune diabetes through multiple mechanisms including the suppression of inflammatory T-cell activity reduction in dendritic cell activation and preservation of pancreatic β-cells. The results support the potential of HBOT as a promising noninvasive adjuvant therapy for the prevention and management of type 1 diabetes in clinical settings meriting further exploration for its efficacy and safety in human trials.

Conclusion

The present study underscores the potent efficacy of hyperbaric oxygen therapy (HBOT) in mitigating the onset of autoimmune diabetes in nonobese diabetic (NOD) mice. Administering daily sessions of HBOT with 100% oxygen at 2.0 ATA for 60 minutes significantly curtailed the incidence of both cyclophosphamide-induced and spontaneous diabetes. Notably treated mice exhibited a marked reduction in insulitis severity decreased T-cell proliferation elevated expression of the regulatory marker CD62L on T cells and diminished expression of costimulatory molecules on dendritic cells. Additionally a favorable shift in β-cell dynamics was observed characterized by reduced apoptosis and enhanced proliferation of insulin-producing cells.

These findings are significant as they highlight the potential of HBOT as a noninvasive adjunctive therapy for the prevention of type 1 diabetes. The therapy’s ability to modulate immune responses and preserve β-cell mass opens new avenues for therapeutic interventions that could delay or even prevent the onset of diabetes. Future research should aim to validate these promising results in clinical trials explore the underlying molecular mechanisms in greater detail and evaluate the long-term benefits and safety of HBOT in human subjects. Such investigations could pave the way for HBOT to become an integral part of diabetes prevention strategies ultimately improving patient outcomes.