Outcome

This study illustrates the promising potential of Hyperbaric Oxygen Therapy (HBO) in preserving cognitive function in a rat model of mild cognitive impairment (MCI). By reducing apoptosis and maintaining healthier hippocampal cell morphology HBO therapy was shown to improve cognitive performance as evidenced by shorter escape latency and a higher number of platform crossings in the Morris water maze test.

Introduction

Hyperbaric oxygen therapy (HBO) has shown promising results in improving cognitive function in a rat model of mild cognitive impairment (MCI). This study aimed to explore the effects of HBO on cognitive performance and delineate the underlying mechanisms with a particular focus on the extracellular-regulated kinase (ERK) signaling pathway. Rats subjected to HBO demonstrated significantly enhanced cognitive abilities in the Morris water maze test exhibiting shorter escape times and a greater number of platform crossings indicative of superior memory and learning capacities. Furthermore HBO-treated rats displayed reduced apoptosis and improved hippocampal cell morphology. Molecular analysis revealed elevated levels of total ERK1/2 and phosphorylated ERK1/2 proteins in the HBO group highlighting the crucial role of the ERK signaling pathway in mediating the observed cognitive benefits. These findings suggest that HBO therapy may protect against early cognitive dysfunction by inhibiting apoptosis through the activation of the ERK pathway offering a potential therapeutic strategy for addressing cognitive decline associated with conditions like MCI.

Results

Rats treated with Hyperbaric Oxygen Therapy (HBO) exhibited significant improvements in cognitive function compared to untreated counterparts in a model of mild cognitive impairment (MCI). In the Morris water maze test HBO-treated rats had significantly shorter escape times and a higher frequency of crossing the platform location indicating enhanced memory and learning abilities.

Biologically HBO-treated rats demonstrated reduced apoptosis and better-preserved hippocampal cell morphology as compared to untreated MCI rats. Analysis showed that the levels of the apoptosis marker caspase 3 were markedly lower in the HBO group. Additionally the HBO group exhibited elevated levels of both total ERK1/2 and phosphorylated ERK1/2 which are pivotal components of the ERK signaling pathway that promote cell survival and neuroprotection.

Importantly the beneficial effects of HBO on cognitive function were partially reversed by the administration of the ERK signaling inhibitor U0126. This suggests that the protective impact of HBO is mediated through the activation of the ERK signaling pathway which plays a critical role in reducing apoptosis and supporting cognitive health.

Overall these findings underscore the potential of HBO therapy in mitigating early cognitive dysfunction through ERK pathway modulation thereby offering a promising therapeutic avenue for conditions such as MCI.

Conclusion

In conclusion this study illustrates the promising potential of Hyperbaric Oxygen Therapy (HBOT) in preserving cognitive function in a rat model of mild cognitive impairment (MCI). Key findings indicate that HBOT significantly enhances cognitive performance evidenced by improved results in the Morris water maze test. The therapy’s benefits appear to be mediated through the ERK signaling pathway as treatment led to reduced apoptosis and healthier hippocampal cell morphology. The involvement of ERK signaling was further corroborated by the partial reversal of cognitive improvements upon the introduction of an ERK inhibitor.

These results underscore the significance of HBOT as a potential therapeutic strategy for early cognitive dysfunction. By effectively reducing cell death and promoting neuroprotection HBOT could play a crucial role in mitigating the effects of MCI. Future research should aim to explore HBOT’s application in human subjects and further elucidate the molecular mechanisms through which it exerts its cognitive benefits potentially paving the way for new targeted interventions in the treatment of cognitive decline.