Cargando…
Prophylactic treatment of hyperbaric oxygen treatment mitigates inflammatory response via mitochondria transfer
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) throu...
Autores principales: | , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2019
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6630002/ https://www.ncbi.nlm.nih.gov/pubmed/30972972 http://dx.doi.org/10.1111/cns.13124 |
_version_ | 1783435206489800704 |
---|---|
author | Lippert, Trenton Borlongan, Cesario V. |
author_facet | Lippert, Trenton Borlongan, Cesario V. |
author_sort | Lippert, Trenton |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-6630002 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-66300022019-08-07 Prophylactic treatment of hyperbaric oxygen treatment mitigates inflammatory response via mitochondria transfer Lippert, Trenton Borlongan, Cesario V. CNS Neurosci Ther Original Articles 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. John Wiley and Sons Inc. 2019-04-11 /pmc/articles/PMC6630002/ /pubmed/30972972 http://dx.doi.org/10.1111/cns.13124 Text en © 2019 The Authors. CNS Neuroscience & Therapeutics Published by John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Lippert, Trenton Borlongan, Cesario V. Prophylactic treatment of hyperbaric oxygen treatment mitigates inflammatory response via mitochondria transfer |
title | Prophylactic treatment of hyperbaric oxygen treatment mitigates inflammatory response via mitochondria transfer |
title_full | Prophylactic treatment of hyperbaric oxygen treatment mitigates inflammatory response via mitochondria transfer |
title_fullStr | Prophylactic treatment of hyperbaric oxygen treatment mitigates inflammatory response via mitochondria transfer |
title_full_unstemmed | Prophylactic treatment of hyperbaric oxygen treatment mitigates inflammatory response via mitochondria transfer |
title_short | Prophylactic treatment of hyperbaric oxygen treatment mitigates inflammatory response via mitochondria transfer |
title_sort | prophylactic treatment of hyperbaric oxygen treatment mitigates inflammatory response via mitochondria transfer |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6630002/ https://www.ncbi.nlm.nih.gov/pubmed/30972972 http://dx.doi.org/10.1111/cns.13124 |
work_keys_str_mv | AT lipperttrenton prophylactictreatmentofhyperbaricoxygentreatmentmitigatesinflammatoryresponseviamitochondriatransfer AT borlongancesariov prophylactictreatmentofhyperbaricoxygentreatmentmitigatesinflammatoryresponseviamitochondriatransfer |