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Buyang Huanwu Decoction promotes the neurological recovery of traumatic spinal cord injury via inhibiting apoptosis, inflammation, and oxidative stress
BACKGROUND: The incidence rate of spinal cord injury (SCI) is increasing, and the mortality or disability rate caused by SCI remains high in the world. Buyang Huanwu Decoction (BYHWD) is a kind of Traditional Chinese medicine, and it is believed to be effective in several kinds of nervous system dis...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10336660/ https://www.ncbi.nlm.nih.gov/pubmed/37506135 http://dx.doi.org/10.1002/iid3.933 |
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author | Li, Xu Song, Yingjun Yang, Yang Zhang, Guofu |
author_facet | Li, Xu Song, Yingjun Yang, Yang Zhang, Guofu |
author_sort | Li, Xu |
collection | PubMed |
description | BACKGROUND: The incidence rate of spinal cord injury (SCI) is increasing, and the mortality or disability rate caused by SCI remains high in the world. Buyang Huanwu Decoction (BYHWD) is a kind of Traditional Chinese medicine, and it is believed to be effective in several kinds of nervous system diseases. Whether BYHWD could improve SCI and the potential function mechanism remain unclear. METHODS: SCI animal model was established by damaging T10 spinal cord. Animals experiments included five groups as follows: Sham, SCI, SCI+BYHWD, SCI+mesenchymal stromal cells (MSCs), and SCI+BYHWD+MSCs. H(2)O(2)‐treated cells (100 µM, 6 h) were used to simulate SCI damage in vitro, which included five groups as follows: control, H(2)O(2), H(2)O(2)+BYHWD, H(2)O(2)+MSCs, and H(2)O(2)+BYHWD+MSCs. The behavioral function was evaluated with Tarlov and inclined plated test score. Western blot analysis and immunohistochemical staining were used to detect protein expression. The levels of superoxide dismutase (SOD), catalase (CAT), malondiadehyde (MDA), interleukin (IL)‐1β, tumor necrosis factor‐α, and IL‐6 in serum were measured with commercial enzyme‐linked immunosorbent assay kits. terminal deoxynucleotidyl transferase dUTP nick end labeling staining and flow cytometry were performed to measure apoptosis in vivo and in vitro levels. Gene expression profiling analysis was performed to analyze differential expression genes. RESULTS: BYHWD suppressed apoptosis and accelerating cell proliferation after SCI. Recovery of neurofunction, inhibition of inflammatory response, and oxidative condition were achieved by BYHWD and MSCs. The expression levels of gp130/Janus kinase/signal transducers and activator of transcription (JAK/STAT) were suppressed by BYHWD and MSCs, both in vivo and in vitro. BYHWD and MSCs markedly promoted cells viability and inhibited apoptosis. Greater gene expression difference was observed between group control and H(2)O(2) through gene expression profiling analysis. The recovery effects of traumatic SCI by BYHWD were similar to MSCs, and synergies effects were observed in several items. CONCLUSION: BYHWD could increase Tarlov score and Basso, Beatie, and Bresnahan functional score, inhibit apoptosis, inflammatory response, and oxidative condition after SCI. The expression level of gp130/JAK/STAT axis was suppressed by BYHWD. BYHWD might be a new therapeutic strategy for the prevention or treatment of SCI. |
format | Online Article Text |
id | pubmed-10336660 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-103366602023-07-13 Buyang Huanwu Decoction promotes the neurological recovery of traumatic spinal cord injury via inhibiting apoptosis, inflammation, and oxidative stress Li, Xu Song, Yingjun Yang, Yang Zhang, Guofu Immun Inflamm Dis Original Articles BACKGROUND: The incidence rate of spinal cord injury (SCI) is increasing, and the mortality or disability rate caused by SCI remains high in the world. Buyang Huanwu Decoction (BYHWD) is a kind of Traditional Chinese medicine, and it is believed to be effective in several kinds of nervous system diseases. Whether BYHWD could improve SCI and the potential function mechanism remain unclear. METHODS: SCI animal model was established by damaging T10 spinal cord. Animals experiments included five groups as follows: Sham, SCI, SCI+BYHWD, SCI+mesenchymal stromal cells (MSCs), and SCI+BYHWD+MSCs. H(2)O(2)‐treated cells (100 µM, 6 h) were used to simulate SCI damage in vitro, which included five groups as follows: control, H(2)O(2), H(2)O(2)+BYHWD, H(2)O(2)+MSCs, and H(2)O(2)+BYHWD+MSCs. The behavioral function was evaluated with Tarlov and inclined plated test score. Western blot analysis and immunohistochemical staining were used to detect protein expression. The levels of superoxide dismutase (SOD), catalase (CAT), malondiadehyde (MDA), interleukin (IL)‐1β, tumor necrosis factor‐α, and IL‐6 in serum were measured with commercial enzyme‐linked immunosorbent assay kits. terminal deoxynucleotidyl transferase dUTP nick end labeling staining and flow cytometry were performed to measure apoptosis in vivo and in vitro levels. Gene expression profiling analysis was performed to analyze differential expression genes. RESULTS: BYHWD suppressed apoptosis and accelerating cell proliferation after SCI. Recovery of neurofunction, inhibition of inflammatory response, and oxidative condition were achieved by BYHWD and MSCs. The expression levels of gp130/Janus kinase/signal transducers and activator of transcription (JAK/STAT) were suppressed by BYHWD and MSCs, both in vivo and in vitro. BYHWD and MSCs markedly promoted cells viability and inhibited apoptosis. Greater gene expression difference was observed between group control and H(2)O(2) through gene expression profiling analysis. The recovery effects of traumatic SCI by BYHWD were similar to MSCs, and synergies effects were observed in several items. CONCLUSION: BYHWD could increase Tarlov score and Basso, Beatie, and Bresnahan functional score, inhibit apoptosis, inflammatory response, and oxidative condition after SCI. The expression level of gp130/JAK/STAT axis was suppressed by BYHWD. BYHWD might be a new therapeutic strategy for the prevention or treatment of SCI. John Wiley and Sons Inc. 2023-07-12 /pmc/articles/PMC10336660/ /pubmed/37506135 http://dx.doi.org/10.1002/iid3.933 Text en © 2023 The Authors. Immunity, Inflammation and Disease published by John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://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 Li, Xu Song, Yingjun Yang, Yang Zhang, Guofu Buyang Huanwu Decoction promotes the neurological recovery of traumatic spinal cord injury via inhibiting apoptosis, inflammation, and oxidative stress |
title | Buyang Huanwu Decoction promotes the neurological recovery of traumatic spinal cord injury via inhibiting apoptosis, inflammation, and oxidative stress |
title_full | Buyang Huanwu Decoction promotes the neurological recovery of traumatic spinal cord injury via inhibiting apoptosis, inflammation, and oxidative stress |
title_fullStr | Buyang Huanwu Decoction promotes the neurological recovery of traumatic spinal cord injury via inhibiting apoptosis, inflammation, and oxidative stress |
title_full_unstemmed | Buyang Huanwu Decoction promotes the neurological recovery of traumatic spinal cord injury via inhibiting apoptosis, inflammation, and oxidative stress |
title_short | Buyang Huanwu Decoction promotes the neurological recovery of traumatic spinal cord injury via inhibiting apoptosis, inflammation, and oxidative stress |
title_sort | buyang huanwu decoction promotes the neurological recovery of traumatic spinal cord injury via inhibiting apoptosis, inflammation, and oxidative stress |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10336660/ https://www.ncbi.nlm.nih.gov/pubmed/37506135 http://dx.doi.org/10.1002/iid3.933 |
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