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Dl‐3‐n‐butylphthalide attenuates acute inflammatory activation in rats with spinal cord injury by inhibiting microglial TLR4/NF‐κB signalling
In this study, we examined the neuroprotective effects and anti‐inflammatory properties of Dl‐3‐n‐butylphthalide (NBP) in Sprague‐Dawley (SD) rats following traumatic spinal cord injury (SCI) as well as microglia activation and inflammatory response both in vivo and in vitro. Our results showed that...
Autores principales: | , , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5661102/ https://www.ncbi.nlm.nih.gov/pubmed/28842949 http://dx.doi.org/10.1111/jcmm.13212 |
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author | He, Zili Zhou, Yulong Lin, Li Wang, Qingqing Khor, Sinan Mao, Yuqin Li, Jiawei Zhen, Zengming Chen, Jian Gao, Zhenzhen Wu, Fenzan Zhang, Xie Zhang, Hongyu Xu, Hua‐Zi Wang, Zhouguang Xiao, Jian |
author_facet | He, Zili Zhou, Yulong Lin, Li Wang, Qingqing Khor, Sinan Mao, Yuqin Li, Jiawei Zhen, Zengming Chen, Jian Gao, Zhenzhen Wu, Fenzan Zhang, Xie Zhang, Hongyu Xu, Hua‐Zi Wang, Zhouguang Xiao, Jian |
author_sort | He, Zili |
collection | PubMed |
description | In this study, we examined the neuroprotective effects and anti‐inflammatory properties of Dl‐3‐n‐butylphthalide (NBP) in Sprague‐Dawley (SD) rats following traumatic spinal cord injury (SCI) as well as microglia activation and inflammatory response both in vivo and in vitro. Our results showed that NBP improved the locomotor recovery of SD rats after SCI an significantly diminished the lesion cavity area of the spinal cord, apoptotic activity in neurons, and the number of TUNEL‐positive cells at 7 days post‐injury. NBP inhibited activation of microglia, diminished the release of inflammatory mediators, and reduced the upregulation of microglial TLR4/NF‐κB expression at 1 day post‐injury. In a co‐culture system with BV‐2 cells and PC12 cells, NBP significantly reduced the cytotoxicity of BV‐2 cells following lipopolysaccharide (LPS) stimulation. In addition, NBP reduced the activation of BV‐2 cells, diminished the release of inflammatory mediators, and inhibited microglial TLR4/NF‐κB expression in BV‐2 cells. Our findings demonstrate that NBP may have neuroprotective and anti‐inflammatory properties in the treatment of SCI by inhibiting the activation of microglia via TLR4/NF‐κB signalling. |
format | Online Article Text |
id | pubmed-5661102 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-56611022017-11-02 Dl‐3‐n‐butylphthalide attenuates acute inflammatory activation in rats with spinal cord injury by inhibiting microglial TLR4/NF‐κB signalling He, Zili Zhou, Yulong Lin, Li Wang, Qingqing Khor, Sinan Mao, Yuqin Li, Jiawei Zhen, Zengming Chen, Jian Gao, Zhenzhen Wu, Fenzan Zhang, Xie Zhang, Hongyu Xu, Hua‐Zi Wang, Zhouguang Xiao, Jian J Cell Mol Med Original Articles In this study, we examined the neuroprotective effects and anti‐inflammatory properties of Dl‐3‐n‐butylphthalide (NBP) in Sprague‐Dawley (SD) rats following traumatic spinal cord injury (SCI) as well as microglia activation and inflammatory response both in vivo and in vitro. Our results showed that NBP improved the locomotor recovery of SD rats after SCI an significantly diminished the lesion cavity area of the spinal cord, apoptotic activity in neurons, and the number of TUNEL‐positive cells at 7 days post‐injury. NBP inhibited activation of microglia, diminished the release of inflammatory mediators, and reduced the upregulation of microglial TLR4/NF‐κB expression at 1 day post‐injury. In a co‐culture system with BV‐2 cells and PC12 cells, NBP significantly reduced the cytotoxicity of BV‐2 cells following lipopolysaccharide (LPS) stimulation. In addition, NBP reduced the activation of BV‐2 cells, diminished the release of inflammatory mediators, and inhibited microglial TLR4/NF‐κB expression in BV‐2 cells. Our findings demonstrate that NBP may have neuroprotective and anti‐inflammatory properties in the treatment of SCI by inhibiting the activation of microglia via TLR4/NF‐κB signalling. John Wiley and Sons Inc. 2017-08-25 2017-11 /pmc/articles/PMC5661102/ /pubmed/28842949 http://dx.doi.org/10.1111/jcmm.13212 Text en © 2017 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine. This is an open access article under the terms of the Creative Commons Attribution (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 He, Zili Zhou, Yulong Lin, Li Wang, Qingqing Khor, Sinan Mao, Yuqin Li, Jiawei Zhen, Zengming Chen, Jian Gao, Zhenzhen Wu, Fenzan Zhang, Xie Zhang, Hongyu Xu, Hua‐Zi Wang, Zhouguang Xiao, Jian Dl‐3‐n‐butylphthalide attenuates acute inflammatory activation in rats with spinal cord injury by inhibiting microglial TLR4/NF‐κB signalling |
title | Dl‐3‐n‐butylphthalide attenuates acute inflammatory activation in rats with spinal cord injury by inhibiting microglial TLR4/NF‐κB signalling |
title_full | Dl‐3‐n‐butylphthalide attenuates acute inflammatory activation in rats with spinal cord injury by inhibiting microglial TLR4/NF‐κB signalling |
title_fullStr | Dl‐3‐n‐butylphthalide attenuates acute inflammatory activation in rats with spinal cord injury by inhibiting microglial TLR4/NF‐κB signalling |
title_full_unstemmed | Dl‐3‐n‐butylphthalide attenuates acute inflammatory activation in rats with spinal cord injury by inhibiting microglial TLR4/NF‐κB signalling |
title_short | Dl‐3‐n‐butylphthalide attenuates acute inflammatory activation in rats with spinal cord injury by inhibiting microglial TLR4/NF‐κB signalling |
title_sort | dl‐3‐n‐butylphthalide attenuates acute inflammatory activation in rats with spinal cord injury by inhibiting microglial tlr4/nf‐κb signalling |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5661102/ https://www.ncbi.nlm.nih.gov/pubmed/28842949 http://dx.doi.org/10.1111/jcmm.13212 |
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