Ossigenoterapia iperbarica (OTI)

Diverse evidenze scientifiche mostrano come l’ossigenoterapia iperbarica (OTI) possa essere utilizzata come precondizionamento ed azione profilattica in diversi quadri clinici.

Questo articolo ulteriormente conferma queste evidenze e si basa su uno studio in vitro su cellule neuronali di ratto. Queste cellule vengono esposte al Tumor necrosis factor (TNFα) o al lipopolisaccaride (LPS) per simulare morte cellulare da stroke o da trauma cerebrale (TBI).
Quando queste cellule vengono esposte a OTI si osserva un incremento della vitalità cellulare mediata dal trasferimento di mitocondri dagli astrociti alle cellule neuronali sofferenti determinando una riduzione dei fenomeni infiammatori.
 
CNS Neurosci Ther. 2019 Apr 11. doi: 10.1111/cns.13124.
Prophylactic treatment of hyperbaric oxygen treatment mitigates inflammatory response via mitochondria transfer.
Lippert T Borlongan
 
AIMS:
Hyperbaric oxygen therapy (HBOT) has been widely used as postinjury treatment; however, we investigate its ability to mitigate potential damage as a preconditioning option. Here, we tested the hypothesis that HBOT preconditioning mitigates cell death in primary rat neuronal cells (PRNCs) through the transfer of mitochondria from astrocytes.


METHODS:
Primary rat neuronal cells were subjected to a 90-minute HBOT treatment at 2.5 absolute atmospheres prior to either tumor necrosis factor-alpha (TNF-alpha) or lipopolysaccharide (LPS) injury to simulate the inflammation-plagued secondary cell death associated with stroke and traumatic brain injury (TBI). After incubation with TNF-alpha or LPS, the cell viability of each group was examined.


RESULTS:
There was a significant increase of cell viability accompanied by mitochondrial transfer in the injury groups that received HBOT preconditioning compared to the injury alone groups (44 ± 5.2 vs 68 ± 4.48, n = 20, P < 0.05). The transfer of mitochondria directly after HBOT treatment was visualized by capturing images in 5-minute intervals, which revealed that the robust transfer of mitochondria begins soon after HBOT and persisted throughout the treatment.


CONCLUSION:
This study shows that HBOT preconditioning stands as a robust prophylactic treatment for sequestration of inflammation inherent in stroke and TBI, possibly facilitating the transfer of resilient mitochondria from astrocytes to inflammation-susceptible neuronal cells in mitigating cell death.

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