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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...

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Detalles Bibliográficos
Autores principales: 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
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2017
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.
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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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