Neuroprotection by diarylpropionitrile in mice with spinal cord injury

The initial impact of spinal cord injury (SCI) often results in inflammation leading to irreversible damage with consequent loss of locomotor function. Minimal recovery is achieved once permanent damage has occurred. Using a mouse model of SCI we observed a transitory increase followed by a rapid de...

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Main Authors:	Suwanna, Nirut, Thangnipon, Wipawan, Kumar, Shalini, de Vellis, Jean
Format:	Online
Language:	English
Published:	Leibniz Research Centre for Working Environment and Human Factors 2014
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4464390/

id	pubmed-4464390
recordtype	oai_dc
spelling	pubmed-44643902015-09-28 Neuroprotection by diarylpropionitrile in mice with spinal cord injury Suwanna, Nirut Thangnipon, Wipawan Kumar, Shalini de Vellis, Jean Original Article The initial impact of spinal cord injury (SCI) often results in inflammation leading to irreversible damage with consequent loss of locomotor function. Minimal recovery is achieved once permanent damage has occurred. Using a mouse model of SCI we observed a transitory increase followed by a rapid decline in gene expression and protein levels of nuclear factor erythroid 2-related factor 2 (Nrf2), a master regulator of cellular anti-oxidative genes. Immediate treatment with diarylpropionitrile (DPN), a non-steroidal selective estrogen receptor ß ligand, resulted in a significant increase in Nrf2 levels, and reduction of inflammation and apoptosis compared to untreated SCI animals. Furthermore, DPN-treatment improved locomotor function within 7 days after induction of SCI. DPN acted through activation of PI3K/ Akt pathway, known to be involved in down-regulation of apoptosis and up-regulation of cell survival in injured tissues. These findings suggest that immediate activation of cellular anti-oxidative stress mechanisms should provide protection against irreversible tissue damage and its profound detrimental effect on locomotor function associated with SCI. Leibniz Research Centre for Working Environment and Human Factors 2014-09-22 /pmc/articles/PMC4464390/ /pubmed/26417324 Text en Copyright © 2014 Suwanna et al. http://www.excli.de/documents/assignment_of_rights.pdf This is an Open Access article distributed under the following Assignment of Rights http://www.excli.de/documents/assignment_of_rights.pdf. You are free to copy, distribute and transmit the work, provided the original author and source are credited.
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Suwanna, Nirut Thangnipon, Wipawan Kumar, Shalini de Vellis, Jean
spellingShingle	Suwanna, Nirut Thangnipon, Wipawan Kumar, Shalini de Vellis, Jean Neuroprotection by diarylpropionitrile in mice with spinal cord injury
author_facet	Suwanna, Nirut Thangnipon, Wipawan Kumar, Shalini de Vellis, Jean
author_sort	Suwanna, Nirut
title	Neuroprotection by diarylpropionitrile in mice with spinal cord injury
title_short	Neuroprotection by diarylpropionitrile in mice with spinal cord injury
title_full	Neuroprotection by diarylpropionitrile in mice with spinal cord injury
title_fullStr	Neuroprotection by diarylpropionitrile in mice with spinal cord injury
title_full_unstemmed	Neuroprotection by diarylpropionitrile in mice with spinal cord injury
title_sort	neuroprotection by diarylpropionitrile in mice with spinal cord injury
description	The initial impact of spinal cord injury (SCI) often results in inflammation leading to irreversible damage with consequent loss of locomotor function. Minimal recovery is achieved once permanent damage has occurred. Using a mouse model of SCI we observed a transitory increase followed by a rapid decline in gene expression and protein levels of nuclear factor erythroid 2-related factor 2 (Nrf2), a master regulator of cellular anti-oxidative genes. Immediate treatment with diarylpropionitrile (DPN), a non-steroidal selective estrogen receptor ß ligand, resulted in a significant increase in Nrf2 levels, and reduction of inflammation and apoptosis compared to untreated SCI animals. Furthermore, DPN-treatment improved locomotor function within 7 days after induction of SCI. DPN acted through activation of PI3K/ Akt pathway, known to be involved in down-regulation of apoptosis and up-regulation of cell survival in injured tissues. These findings suggest that immediate activation of cellular anti-oxidative stress mechanisms should provide protection against irreversible tissue damage and its profound detrimental effect on locomotor function associated with SCI.
publisher	Leibniz Research Centre for Working Environment and Human Factors
publishDate	2014
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4464390/
_version_	1613234746533347328

Neuroprotection by diarylpropionitrile in mice with spinal cord injury

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