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Dl-3-n-butylphthalide prevents the disruption of blood-spinal cord barrier via inhibiting endoplasmic reticulum stress following spinal cord injury

After spinal cord injury (SCI), the destruction of blood-spinal cord barrier (BSCB) is shown to accelerate gathering of noxious blood-derived components in the nervous system, leading to secondary neurodegenerative damages. SCI activates endoplasmic reticulum stress (ER stress), which is considered...

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Autores principales: Zheng, Binbin, Zhou, Yulong, Zhang, Hongyu, Yang, Guangyong, Hong, Zhenghua, Han, Dandan, Wang, Qingqing, He, Zili, Liu, Yanlong, Wu, Fenzan, Zhang, Xie, Tong, Songlin, Xu, Huazi, Xiao, Jian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Ivyspring International Publisher 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5723918/
https://www.ncbi.nlm.nih.gov/pubmed/29230100
http://dx.doi.org/10.7150/ijbs.21107
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author Zheng, Binbin
Zhou, Yulong
Zhang, Hongyu
Yang, Guangyong
Hong, Zhenghua
Han, Dandan
Wang, Qingqing
He, Zili
Liu, Yanlong
Wu, Fenzan
Zhang, Xie
Tong, Songlin
Xu, Huazi
Xiao, Jian
author_facet Zheng, Binbin
Zhou, Yulong
Zhang, Hongyu
Yang, Guangyong
Hong, Zhenghua
Han, Dandan
Wang, Qingqing
He, Zili
Liu, Yanlong
Wu, Fenzan
Zhang, Xie
Tong, Songlin
Xu, Huazi
Xiao, Jian
author_sort Zheng, Binbin
collection PubMed
description After spinal cord injury (SCI), the destruction of blood-spinal cord barrier (BSCB) is shown to accelerate gathering of noxious blood-derived components in the nervous system, leading to secondary neurodegenerative damages. SCI activates endoplasmic reticulum stress (ER stress), which is considered to evoke secondary damages of neurons and glia. Recent evidence indicates that Dl-3-n-butylphthalide (NBP) has the neuroprotective effect in ischaemic brain injury, but whether it has protective effects on SCI or not is largely unclear. Here, we show that NBP prevented BSCB disruption after SCI via inhibition of ER stress. Following a moderate contusion injury of the T9 level of spinal cord, NBP was administered by oral gavage and further treated once a day. NBP significantly attenuated BSCB permeability and breakdown of adherens junction (AJ) and tight junction (TJ) proteins, then improved locomotion recovery following SCI. The protective role of NBP on BSCB disruption is associated with the restrain of ER stress caused by SCI. Furthermore, NBP considerably constrained the expression of ER stress-associated proteins and degradation of TJ and AJ in human brain microvascular endothelial cells (HBMECs) treated with TG. In conclusion, our results indicate that ER stress is associated with the disruption of BSCB integrity after injury, NBP attenuates BSCB disruption via inhibiting ER stress and improve functional recovery following SCI.
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spelling pubmed-57239182017-12-11 Dl-3-n-butylphthalide prevents the disruption of blood-spinal cord barrier via inhibiting endoplasmic reticulum stress following spinal cord injury Zheng, Binbin Zhou, Yulong Zhang, Hongyu Yang, Guangyong Hong, Zhenghua Han, Dandan Wang, Qingqing He, Zili Liu, Yanlong Wu, Fenzan Zhang, Xie Tong, Songlin Xu, Huazi Xiao, Jian Int J Biol Sci Research Paper After spinal cord injury (SCI), the destruction of blood-spinal cord barrier (BSCB) is shown to accelerate gathering of noxious blood-derived components in the nervous system, leading to secondary neurodegenerative damages. SCI activates endoplasmic reticulum stress (ER stress), which is considered to evoke secondary damages of neurons and glia. Recent evidence indicates that Dl-3-n-butylphthalide (NBP) has the neuroprotective effect in ischaemic brain injury, but whether it has protective effects on SCI or not is largely unclear. Here, we show that NBP prevented BSCB disruption after SCI via inhibition of ER stress. Following a moderate contusion injury of the T9 level of spinal cord, NBP was administered by oral gavage and further treated once a day. NBP significantly attenuated BSCB permeability and breakdown of adherens junction (AJ) and tight junction (TJ) proteins, then improved locomotion recovery following SCI. The protective role of NBP on BSCB disruption is associated with the restrain of ER stress caused by SCI. Furthermore, NBP considerably constrained the expression of ER stress-associated proteins and degradation of TJ and AJ in human brain microvascular endothelial cells (HBMECs) treated with TG. In conclusion, our results indicate that ER stress is associated with the disruption of BSCB integrity after injury, NBP attenuates BSCB disruption via inhibiting ER stress and improve functional recovery following SCI. Ivyspring International Publisher 2017-11-27 /pmc/articles/PMC5723918/ /pubmed/29230100 http://dx.doi.org/10.7150/ijbs.21107 Text en © Ivyspring International Publisher This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) license (https://creativecommons.org/licenses/by-nc/4.0/). See http://ivyspring.com/terms for full terms and conditions.
spellingShingle Research Paper
Zheng, Binbin
Zhou, Yulong
Zhang, Hongyu
Yang, Guangyong
Hong, Zhenghua
Han, Dandan
Wang, Qingqing
He, Zili
Liu, Yanlong
Wu, Fenzan
Zhang, Xie
Tong, Songlin
Xu, Huazi
Xiao, Jian
Dl-3-n-butylphthalide prevents the disruption of blood-spinal cord barrier via inhibiting endoplasmic reticulum stress following spinal cord injury
title Dl-3-n-butylphthalide prevents the disruption of blood-spinal cord barrier via inhibiting endoplasmic reticulum stress following spinal cord injury
title_full Dl-3-n-butylphthalide prevents the disruption of blood-spinal cord barrier via inhibiting endoplasmic reticulum stress following spinal cord injury
title_fullStr Dl-3-n-butylphthalide prevents the disruption of blood-spinal cord barrier via inhibiting endoplasmic reticulum stress following spinal cord injury
title_full_unstemmed Dl-3-n-butylphthalide prevents the disruption of blood-spinal cord barrier via inhibiting endoplasmic reticulum stress following spinal cord injury
title_short Dl-3-n-butylphthalide prevents the disruption of blood-spinal cord barrier via inhibiting endoplasmic reticulum stress following spinal cord injury
title_sort dl-3-n-butylphthalide prevents the disruption of blood-spinal cord barrier via inhibiting endoplasmic reticulum stress following spinal cord injury
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5723918/
https://www.ncbi.nlm.nih.gov/pubmed/29230100
http://dx.doi.org/10.7150/ijbs.21107
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