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EA participates in pain transition through regulating KCC2 expression by BDNF-TrkB in the spinal cord dorsal horn of male rats
The pathogenesis of chronic pain is complex and poorly treated, seriously affecting the quality of life of patients. Electroacupuncture (EA) relieves pain by preventing the transition of acute pain into chronic pain, but its mechanism of action is still unclear. Here, we aimed to investigate whether...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9982673/ https://www.ncbi.nlm.nih.gov/pubmed/36875547 http://dx.doi.org/10.1016/j.ynpai.2023.100115 |
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author | Shi, Mengting Zhou, Jie Hu, Rong Xu, Haipeng Chen, Yi Wu, Xingying Chen, Bowen Ma, Ruijie |
author_facet | Shi, Mengting Zhou, Jie Hu, Rong Xu, Haipeng Chen, Yi Wu, Xingying Chen, Bowen Ma, Ruijie |
author_sort | Shi, Mengting |
collection | PubMed |
description | The pathogenesis of chronic pain is complex and poorly treated, seriously affecting the quality of life of patients. Electroacupuncture (EA) relieves pain by preventing the transition of acute pain into chronic pain, but its mechanism of action is still unclear. Here, we aimed to investigate whether EA can inhibit pain transition by increasing KCC2 expression via BDNF-TrkB. We used hyperalgesic priming (HP) model to investigate the potential central mechanisms of EA intervention on pain transition. HP model male rats showed significant and persistent mechanically abnormal pain. Brain derived neurotrophic factor (BDNF) expression and Tropomyosin receptor kinase B (TrkB) phosphorylation were upregulated in the affected spinal cord dorsal horn (SCDH) of HP model rats, accompanied by K(+)-Cl(-)- Cotransporter-2 (KCC2) expression was down-regulated. EA significantly increased the mechanical pain threshold in HP model male rats and decreased BDNF and p-TrkB overexpression and upregulated KCC2 expression. Blockade of BDNF with BDNF neutralizing antibody attenuated mechanical abnormal pain in HP rats. Finally, administration of exogenous BDNF by pharmacological methods reversed the EA-induced resistance to abnormal pain. In all, these results suggest that BDNF-TrkB contributes to mechanical abnormal pain in HP model rats and that EA ameliorates mechanical abnormal pain through upregulation of KCC2 by BDNF-TrkB in SCDH. Our study further supports EA as an effective treatment to prevent the transition of acute pain into chronic pain. |
format | Online Article Text |
id | pubmed-9982673 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Elsevier |
record_format | MEDLINE/PubMed |
spelling | pubmed-99826732023-03-04 EA participates in pain transition through regulating KCC2 expression by BDNF-TrkB in the spinal cord dorsal horn of male rats Shi, Mengting Zhou, Jie Hu, Rong Xu, Haipeng Chen, Yi Wu, Xingying Chen, Bowen Ma, Ruijie Neurobiol Pain Original Research Article The pathogenesis of chronic pain is complex and poorly treated, seriously affecting the quality of life of patients. Electroacupuncture (EA) relieves pain by preventing the transition of acute pain into chronic pain, but its mechanism of action is still unclear. Here, we aimed to investigate whether EA can inhibit pain transition by increasing KCC2 expression via BDNF-TrkB. We used hyperalgesic priming (HP) model to investigate the potential central mechanisms of EA intervention on pain transition. HP model male rats showed significant and persistent mechanically abnormal pain. Brain derived neurotrophic factor (BDNF) expression and Tropomyosin receptor kinase B (TrkB) phosphorylation were upregulated in the affected spinal cord dorsal horn (SCDH) of HP model rats, accompanied by K(+)-Cl(-)- Cotransporter-2 (KCC2) expression was down-regulated. EA significantly increased the mechanical pain threshold in HP model male rats and decreased BDNF and p-TrkB overexpression and upregulated KCC2 expression. Blockade of BDNF with BDNF neutralizing antibody attenuated mechanical abnormal pain in HP rats. Finally, administration of exogenous BDNF by pharmacological methods reversed the EA-induced resistance to abnormal pain. In all, these results suggest that BDNF-TrkB contributes to mechanical abnormal pain in HP model rats and that EA ameliorates mechanical abnormal pain through upregulation of KCC2 by BDNF-TrkB in SCDH. Our study further supports EA as an effective treatment to prevent the transition of acute pain into chronic pain. Elsevier 2023-01-05 /pmc/articles/PMC9982673/ /pubmed/36875547 http://dx.doi.org/10.1016/j.ynpai.2023.100115 Text en © 2023 Published by Elsevier Inc. https://creativecommons.org/licenses/by/4.0/This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Original Research Article Shi, Mengting Zhou, Jie Hu, Rong Xu, Haipeng Chen, Yi Wu, Xingying Chen, Bowen Ma, Ruijie EA participates in pain transition through regulating KCC2 expression by BDNF-TrkB in the spinal cord dorsal horn of male rats |
title | EA participates in pain transition through regulating KCC2 expression by BDNF-TrkB in the spinal cord dorsal horn of male rats |
title_full | EA participates in pain transition through regulating KCC2 expression by BDNF-TrkB in the spinal cord dorsal horn of male rats |
title_fullStr | EA participates in pain transition through regulating KCC2 expression by BDNF-TrkB in the spinal cord dorsal horn of male rats |
title_full_unstemmed | EA participates in pain transition through regulating KCC2 expression by BDNF-TrkB in the spinal cord dorsal horn of male rats |
title_short | EA participates in pain transition through regulating KCC2 expression by BDNF-TrkB in the spinal cord dorsal horn of male rats |
title_sort | ea participates in pain transition through regulating kcc2 expression by bdnf-trkb in the spinal cord dorsal horn of male rats |
topic | Original Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9982673/ https://www.ncbi.nlm.nih.gov/pubmed/36875547 http://dx.doi.org/10.1016/j.ynpai.2023.100115 |
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