Ferulic Acid Improves Functional Recovery after Acute Spinal Cord Injury in Rats by Inducing Hypoxia to Inhibit microRNA-590 and Elevate Vascular Endothelial Growth Factor Expressions

Spinal cord injury (SCI) is the leading cause of paralysis, disability and even death in severe cases, and neural stem cells (NSCs) transplant has been employed for repairing SCI. Ferulic acid (FA) is able to promote neurogenesis in various stem cell therapies. We aimed to investigate the effect of...

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Autores principales: Zhenjie Li, Shengyun Wang, Wenfang Li, Hongbin Yuan
Formato: Artículo
Lenguaje:English
Publicado: Frontiers Media S.A. 2017-06-01
Colección:Frontiers in Molecular Neuroscience
Materias:
Acceso en línea:http://journal.frontiersin.org/article/10.3389/fnmol.2017.00183/full
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author Zhenjie Li
Shengyun Wang
Wenfang Li
Hongbin Yuan
author_facet Zhenjie Li
Shengyun Wang
Wenfang Li
Hongbin Yuan
author_sort Zhenjie Li
collection DOAJ
description Spinal cord injury (SCI) is the leading cause of paralysis, disability and even death in severe cases, and neural stem cells (NSCs) transplant has been employed for repairing SCI. Ferulic acid (FA) is able to promote neurogenesis in various stem cell therapies. We aimed to investigate the effect of FA on NSC transplant therapy, and the underlying mechanism, in improving functional recovery in SCI rat model. A rat model of SCI was established, which then received transplant of NSCs with or without FA pre-treatment. Functional recovery of the SCI rats was then evaluated, in terms of spinal cord water content, myeloperoxidase activity and behavioral assessments. Effect of FA in inducing hypoxia in NSCs was also assessed, followed by identifying the hypoxic regulated microRNA and the subsequent target gene. Transplant of FA pre-treated NSCs improved functional recovery of SCI rats to a more significant extent than NSCs without FA pre-treatment. The beneficial effects of FA in repairing SCI was mediated by inducing hypoxia in NSCs, which in turn inhibited microRNA-590 to elevate vascular endothelial growth factor expression. Our findings support the clinical potential of FA in improving efficacy of NSC transplant therapy for treatment of SCI.
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spelling doaj.art-dfb80a9c68f34c0f8bd8752f635f10b42022-12-22T02:05:52ZengFrontiers Media S.A.Frontiers in Molecular Neuroscience1662-50992017-06-011010.3389/fnmol.2017.00183273980Ferulic Acid Improves Functional Recovery after Acute Spinal Cord Injury in Rats by Inducing Hypoxia to Inhibit microRNA-590 and Elevate Vascular Endothelial Growth Factor ExpressionsZhenjie Li0Shengyun Wang1Wenfang Li2Hongbin Yuan3Department of Anesthesiology, Shanghai Changzheng Hospital, The Second Military Medical UniversityShanghai, ChinaDepartment of Emergency and Critical Care Medicine, Shanghai Changzheng Hospital, The Second Military Medical UniversityShanghai, ChinaDepartment of Emergency and Critical Care Medicine, Shanghai Changzheng Hospital, The Second Military Medical UniversityShanghai, ChinaDepartment of Anesthesiology, Shanghai Changzheng Hospital, The Second Military Medical UniversityShanghai, ChinaSpinal cord injury (SCI) is the leading cause of paralysis, disability and even death in severe cases, and neural stem cells (NSCs) transplant has been employed for repairing SCI. Ferulic acid (FA) is able to promote neurogenesis in various stem cell therapies. We aimed to investigate the effect of FA on NSC transplant therapy, and the underlying mechanism, in improving functional recovery in SCI rat model. A rat model of SCI was established, which then received transplant of NSCs with or without FA pre-treatment. Functional recovery of the SCI rats was then evaluated, in terms of spinal cord water content, myeloperoxidase activity and behavioral assessments. Effect of FA in inducing hypoxia in NSCs was also assessed, followed by identifying the hypoxic regulated microRNA and the subsequent target gene. Transplant of FA pre-treated NSCs improved functional recovery of SCI rats to a more significant extent than NSCs without FA pre-treatment. The beneficial effects of FA in repairing SCI was mediated by inducing hypoxia in NSCs, which in turn inhibited microRNA-590 to elevate vascular endothelial growth factor expression. Our findings support the clinical potential of FA in improving efficacy of NSC transplant therapy for treatment of SCI.http://journal.frontiersin.org/article/10.3389/fnmol.2017.00183/fullFerulic acidspinal cord injuryneural stem cellshypoxianeurogenesis
spellingShingle Zhenjie Li
Shengyun Wang
Wenfang Li
Hongbin Yuan
Ferulic Acid Improves Functional Recovery after Acute Spinal Cord Injury in Rats by Inducing Hypoxia to Inhibit microRNA-590 and Elevate Vascular Endothelial Growth Factor Expressions
Frontiers in Molecular Neuroscience
Ferulic acid
spinal cord injury
neural stem cells
hypoxia
neurogenesis
title Ferulic Acid Improves Functional Recovery after Acute Spinal Cord Injury in Rats by Inducing Hypoxia to Inhibit microRNA-590 and Elevate Vascular Endothelial Growth Factor Expressions
title_full Ferulic Acid Improves Functional Recovery after Acute Spinal Cord Injury in Rats by Inducing Hypoxia to Inhibit microRNA-590 and Elevate Vascular Endothelial Growth Factor Expressions
title_fullStr Ferulic Acid Improves Functional Recovery after Acute Spinal Cord Injury in Rats by Inducing Hypoxia to Inhibit microRNA-590 and Elevate Vascular Endothelial Growth Factor Expressions
title_full_unstemmed Ferulic Acid Improves Functional Recovery after Acute Spinal Cord Injury in Rats by Inducing Hypoxia to Inhibit microRNA-590 and Elevate Vascular Endothelial Growth Factor Expressions
title_short Ferulic Acid Improves Functional Recovery after Acute Spinal Cord Injury in Rats by Inducing Hypoxia to Inhibit microRNA-590 and Elevate Vascular Endothelial Growth Factor Expressions
title_sort ferulic acid improves functional recovery after acute spinal cord injury in rats by inducing hypoxia to inhibit microrna 590 and elevate vascular endothelial growth factor expressions
topic Ferulic acid
spinal cord injury
neural stem cells
hypoxia
neurogenesis
url http://journal.frontiersin.org/article/10.3389/fnmol.2017.00183/full
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