Outcome

This study illustrates the promising potential of hyperbaric oxygen (HBO) therapy in protecting against myocardial ischemia-reperfusion injury (MIRI) by targeting mitochondrial dysfunction and autophagy. Conducted on rats the findings report that HBO pretreatment over 14 days significantly improved mitochondrial morphology energy metabolism and cellular health.

Introduction

Hyperbaric oxygen (HBO) therapy has shown promising potential in improving heart function after myocardial ischemia-reperfusion injury (MIRI) a condition caused by the temporary blockage of blood supply to the heart. This study investigates the effects of HBO therapy on mitochondrial function and autophagy two critical factors in cellular health. Over a span of 14 days rats received HBO treatments in a 0.25 MPa chamber. The results revealed significant improvements in mitochondrial morphology and function characterized by increased levels of ATP and energy charge as well as decreased reactive oxygen species and autophagic vesicles. Additionally HBO therapy regulated key genes and proteins related to mitochondrial health and autophagy enhancing beneficial ones like eIF4E‑binding protein 1 mTOR mitofusin 1 and mitofusin 2 while reducing harmful expressions such as Atg5 and p53. These findings suggest that HBO therapy could be an effective treatment to protect heart cells from damage following a heart attack by restoring mitochondrial function and reducing autophagy offering new avenues for therapeutic intervention.

Results

The study investigated the impact of hyperbaric oxygen (HBO) therapy on heart cell health following myocardial ischemia-reperfusion injury (MIRI) by examining its effects on mitochondrial function and autophagy. Over a period of 14 days rats received HBO treatments in a 0.25 MPa chamber revealing noteworthy findings.

HBO therapy notably enhanced mitochondrial morphology and function. The treatment increased levels of ATP and ADP key energy molecules while decreasing AMP and cytochrome c. This improvement in energy metabolism was accompanied by a reduction in reactive oxygen species and autophagic vesicles indicating a decrease in both oxidative stress and cellular self-digestion processes.

Gene and protein analyses further supported these observations. HBO therapy upregulated beneficial proteins and genes including eIF4E‑binding protein 1 mTOR mitochondrial DNA NADH dehydrogenase subunit 1 mitofusin 1 and mitofusin 2. Conversely it downregulated harmful ones such as Atg5 cytochrome c dynamin‑related protein 1 and p53 highlighting the therapy’s role in supporting mitochondrial integrity and reducing autophagy.

The comprehensive impact of HBO therapy on mitochondrial health suggests a protective mechanism against heart cell damage post-MIRI. By enhancing mitochondrial function and inhibiting excessive autophagy HBO provides a promising therapeutic avenue for reducing heart damage after a heart attack. The data offer robust evidence of HBO’s potential to improve cellular and mitochondrial health pointing to its beneficial role in heart disease treatment.

Conclusion

In summary this study underscores the potential of hyperbaric oxygen (HBO) therapy as an effective intervention for myocardial ischemia-reperfusion injury (MIRI) primarily through its positive impact on mitochondrial function and autophagy regulation. Over the course of 14 days HBO treatment notably enhanced mitochondrial health by improving ATP production and morphological stability while reducing oxidative stress and the prevalence of autophagic vesicles. The upregulation of beneficial genes and proteins alongside a reduction of deleterious ones further substantiates HBO’s role in cellular protection and energy metabolism regulation. These promising findings suggest that HBO therapy could be a valuable strategy in reducing heart damage post-heart attack setting the stage for future research to explore its clinical applications and optimize treatment protocols for broader cardiac care.