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Ultrashortwave radiation promotes the recovery of spinal cord injury by inhibiting inflammation via suppression of the MK2/TNF-α pathway
Mitogen-activated protein kinase-activated protein kinase 2 (MK2) and its mediated inflammation are involved in various diseases, including spinal cord injury (SCI). Ultrashortwave (USW) radiation has previously been reported to exert a protective effect on SCI. In the present study, through a serie...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6108855/ https://www.ncbi.nlm.nih.gov/pubmed/30066830 http://dx.doi.org/10.3892/ijmm.2018.3786 |
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author | Wang, Nan Feng, Zhiping Zhao, Wei Zhang, Zhiqiang Zhang, Lixin |
author_facet | Wang, Nan Feng, Zhiping Zhao, Wei Zhang, Zhiqiang Zhang, Lixin |
author_sort | Wang, Nan |
collection | PubMed |
description | Mitogen-activated protein kinase-activated protein kinase 2 (MK2) and its mediated inflammation are involved in various diseases, including spinal cord injury (SCI). Ultrashortwave (USW) radiation has previously been reported to exert a protective effect on SCI. In the present study, through a series of reverse transcription-quantitative polymerase chain reaction (RT-qPCR), western blot and immunofluorescence assay, it was found that MK2 and tumor necrosis factor (TNF)-α/interleukin (IL)-1β were elevated in patients with SCI and in H(2)O(2)-treated C8-D1A cells. Through gene level and protein level detection by using of RT-qPCR, western blot, immunofluorescence assay and terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling assay, it was demonstrated that USW radiation inhibited the expression of MK2/TNF-α/IL-1β and suppressed the apoptosis of H(2)O(2)-treated C8-D1A cells. Furthermore, it was confirmed that the overexpression of MK2 reversed the protective effect of USW on C8-D1A cells, which indicated that USW achieved its function via regulation of the MK2/TNF-α/IL-1β pathway. Finally, using a constructed in vivo model and a series of RT-qPCR, western blot and IHC detection, it was confirmed that USW suppressed the expression of MK2 to promote functional recovery following SCI. The findings of the present study may provide a novel target and improve on the current understanding of how USW functions in the treatment of SCI. |
format | Online Article Text |
id | pubmed-6108855 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-61088552018-08-27 Ultrashortwave radiation promotes the recovery of spinal cord injury by inhibiting inflammation via suppression of the MK2/TNF-α pathway Wang, Nan Feng, Zhiping Zhao, Wei Zhang, Zhiqiang Zhang, Lixin Int J Mol Med Articles Mitogen-activated protein kinase-activated protein kinase 2 (MK2) and its mediated inflammation are involved in various diseases, including spinal cord injury (SCI). Ultrashortwave (USW) radiation has previously been reported to exert a protective effect on SCI. In the present study, through a series of reverse transcription-quantitative polymerase chain reaction (RT-qPCR), western blot and immunofluorescence assay, it was found that MK2 and tumor necrosis factor (TNF)-α/interleukin (IL)-1β were elevated in patients with SCI and in H(2)O(2)-treated C8-D1A cells. Through gene level and protein level detection by using of RT-qPCR, western blot, immunofluorescence assay and terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling assay, it was demonstrated that USW radiation inhibited the expression of MK2/TNF-α/IL-1β and suppressed the apoptosis of H(2)O(2)-treated C8-D1A cells. Furthermore, it was confirmed that the overexpression of MK2 reversed the protective effect of USW on C8-D1A cells, which indicated that USW achieved its function via regulation of the MK2/TNF-α/IL-1β pathway. Finally, using a constructed in vivo model and a series of RT-qPCR, western blot and IHC detection, it was confirmed that USW suppressed the expression of MK2 to promote functional recovery following SCI. The findings of the present study may provide a novel target and improve on the current understanding of how USW functions in the treatment of SCI. D.A. Spandidos 2018-10 2018-07-19 /pmc/articles/PMC6108855/ /pubmed/30066830 http://dx.doi.org/10.3892/ijmm.2018.3786 Text en Copyright: © Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Wang, Nan Feng, Zhiping Zhao, Wei Zhang, Zhiqiang Zhang, Lixin Ultrashortwave radiation promotes the recovery of spinal cord injury by inhibiting inflammation via suppression of the MK2/TNF-α pathway |
title | Ultrashortwave radiation promotes the recovery of spinal cord injury by inhibiting inflammation via suppression of the MK2/TNF-α pathway |
title_full | Ultrashortwave radiation promotes the recovery of spinal cord injury by inhibiting inflammation via suppression of the MK2/TNF-α pathway |
title_fullStr | Ultrashortwave radiation promotes the recovery of spinal cord injury by inhibiting inflammation via suppression of the MK2/TNF-α pathway |
title_full_unstemmed | Ultrashortwave radiation promotes the recovery of spinal cord injury by inhibiting inflammation via suppression of the MK2/TNF-α pathway |
title_short | Ultrashortwave radiation promotes the recovery of spinal cord injury by inhibiting inflammation via suppression of the MK2/TNF-α pathway |
title_sort | ultrashortwave radiation promotes the recovery of spinal cord injury by inhibiting inflammation via suppression of the mk2/tnf-α pathway |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6108855/ https://www.ncbi.nlm.nih.gov/pubmed/30066830 http://dx.doi.org/10.3892/ijmm.2018.3786 |
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