Cargando…
Reactive Oxygen Species Mediate Low Back Pain by Upregulating Substance P in Intervertebral Disc Degeneration
Reactive oxygen species (ROS) are thought to have a strong correlation with a number of intervertebral disc (IVD) diseases. Here, we aimed to determine whether ROS represent an etiology of low back pain (LBP) during IVD degeneration. Thirty degenerated intervertebral disc samples were obtained from...
Autores principales: | , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2021
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8140854/ https://www.ncbi.nlm.nih.gov/pubmed/34093962 http://dx.doi.org/10.1155/2021/6681815 |
_version_ | 1783696259680305152 |
---|---|
author | Zheng, Jiancheng Zhang, Jian Zhang, Xingkai Guo, Zhiping Wu, Wenjian Chen, Zhe Li, Jitian |
author_facet | Zheng, Jiancheng Zhang, Jian Zhang, Xingkai Guo, Zhiping Wu, Wenjian Chen, Zhe Li, Jitian |
author_sort | Zheng, Jiancheng |
collection | PubMed |
description | Reactive oxygen species (ROS) are thought to have a strong correlation with a number of intervertebral disc (IVD) diseases. Here, we aimed to determine whether ROS represent an etiology of low back pain (LBP) during IVD degeneration. Thirty degenerated intervertebral disc samples were obtained from patients, and ROS levels were quantified using dihydroethidium (DHE) staining. The results suggested a significant correlation between the ROS level and the severity of LBP. Subsequently, a puncture-induced LBP model was established in rats, and ROS levels significantly increased compared with those in the sham surgery group, accompanied with severe puncture-induced IVD degeneration. In addition, when ROS levels were increased by H(2)O(2) administration or decreased by NAC treatment, the rats showed increased or decreased LBP, respectively. Based on this evidence, we further determined that stimulation with H(2)O(2) in nucleus pulposus cells (NPCs) in vivo or in vitro resulted in upregulation of substance P (SP), a peptide thought to be involved in the synaptic transmission of pain, and that the severity of LBP decreased when SP levels were increased by exogenous SP administration or neutralized via aprepitant treatment in the IVDs of rats. In conclusion, ROS are primary inducers of LBP based on clinical and animal data, and the mechanism involves ROS stimulation of NPCs to secrete SP, which is a critical neurotransmitter peptide, to promote LBP in IVDs. Therefore, reducing the level of ROS with specific drugs and inhibiting SP may be alternative methods to treat LBP in the clinic. |
format | Online Article Text |
id | pubmed-8140854 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-81408542021-06-04 Reactive Oxygen Species Mediate Low Back Pain by Upregulating Substance P in Intervertebral Disc Degeneration Zheng, Jiancheng Zhang, Jian Zhang, Xingkai Guo, Zhiping Wu, Wenjian Chen, Zhe Li, Jitian Oxid Med Cell Longev Research Article Reactive oxygen species (ROS) are thought to have a strong correlation with a number of intervertebral disc (IVD) diseases. Here, we aimed to determine whether ROS represent an etiology of low back pain (LBP) during IVD degeneration. Thirty degenerated intervertebral disc samples were obtained from patients, and ROS levels were quantified using dihydroethidium (DHE) staining. The results suggested a significant correlation between the ROS level and the severity of LBP. Subsequently, a puncture-induced LBP model was established in rats, and ROS levels significantly increased compared with those in the sham surgery group, accompanied with severe puncture-induced IVD degeneration. In addition, when ROS levels were increased by H(2)O(2) administration or decreased by NAC treatment, the rats showed increased or decreased LBP, respectively. Based on this evidence, we further determined that stimulation with H(2)O(2) in nucleus pulposus cells (NPCs) in vivo or in vitro resulted in upregulation of substance P (SP), a peptide thought to be involved in the synaptic transmission of pain, and that the severity of LBP decreased when SP levels were increased by exogenous SP administration or neutralized via aprepitant treatment in the IVDs of rats. In conclusion, ROS are primary inducers of LBP based on clinical and animal data, and the mechanism involves ROS stimulation of NPCs to secrete SP, which is a critical neurotransmitter peptide, to promote LBP in IVDs. Therefore, reducing the level of ROS with specific drugs and inhibiting SP may be alternative methods to treat LBP in the clinic. Hindawi 2021-05-14 /pmc/articles/PMC8140854/ /pubmed/34093962 http://dx.doi.org/10.1155/2021/6681815 Text en Copyright © 2021 Jiancheng Zheng et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Zheng, Jiancheng Zhang, Jian Zhang, Xingkai Guo, Zhiping Wu, Wenjian Chen, Zhe Li, Jitian Reactive Oxygen Species Mediate Low Back Pain by Upregulating Substance P in Intervertebral Disc Degeneration |
title | Reactive Oxygen Species Mediate Low Back Pain by Upregulating Substance P in Intervertebral Disc Degeneration |
title_full | Reactive Oxygen Species Mediate Low Back Pain by Upregulating Substance P in Intervertebral Disc Degeneration |
title_fullStr | Reactive Oxygen Species Mediate Low Back Pain by Upregulating Substance P in Intervertebral Disc Degeneration |
title_full_unstemmed | Reactive Oxygen Species Mediate Low Back Pain by Upregulating Substance P in Intervertebral Disc Degeneration |
title_short | Reactive Oxygen Species Mediate Low Back Pain by Upregulating Substance P in Intervertebral Disc Degeneration |
title_sort | reactive oxygen species mediate low back pain by upregulating substance p in intervertebral disc degeneration |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8140854/ https://www.ncbi.nlm.nih.gov/pubmed/34093962 http://dx.doi.org/10.1155/2021/6681815 |
work_keys_str_mv | AT zhengjiancheng reactiveoxygenspeciesmediatelowbackpainbyupregulatingsubstancepinintervertebraldiscdegeneration AT zhangjian reactiveoxygenspeciesmediatelowbackpainbyupregulatingsubstancepinintervertebraldiscdegeneration AT zhangxingkai reactiveoxygenspeciesmediatelowbackpainbyupregulatingsubstancepinintervertebraldiscdegeneration AT guozhiping reactiveoxygenspeciesmediatelowbackpainbyupregulatingsubstancepinintervertebraldiscdegeneration AT wuwenjian reactiveoxygenspeciesmediatelowbackpainbyupregulatingsubstancepinintervertebraldiscdegeneration AT chenzhe reactiveoxygenspeciesmediatelowbackpainbyupregulatingsubstancepinintervertebraldiscdegeneration AT lijitian reactiveoxygenspeciesmediatelowbackpainbyupregulatingsubstancepinintervertebraldiscdegeneration |