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Administration of Protocatechuic Acid Reduces Traumatic Brain Injury-Induced Neuronal Death

Protocatechuic acid (PCA) was first purified from green tea and has shown numerous biological activities, including anti-apoptotic, anti-inflammatory, and anti-atherosclerotic effects. The effect of PCA on traumatic brain injury (TBI)-induced neuronal death has not previously been evaluated. TBI is...

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Autores principales: Lee, Sang Hwon, Choi, Bo Young, Lee, Song Hee, Kho, A. Ra, Jeong, Jeong Hyun, Hong, Dae Ki, Suh, Sang Won
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5751113/
https://www.ncbi.nlm.nih.gov/pubmed/29168791
http://dx.doi.org/10.3390/ijms18122510
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author Lee, Sang Hwon
Choi, Bo Young
Lee, Song Hee
Kho, A. Ra
Jeong, Jeong Hyun
Hong, Dae Ki
Suh, Sang Won
author_facet Lee, Sang Hwon
Choi, Bo Young
Lee, Song Hee
Kho, A. Ra
Jeong, Jeong Hyun
Hong, Dae Ki
Suh, Sang Won
author_sort Lee, Sang Hwon
collection PubMed
description Protocatechuic acid (PCA) was first purified from green tea and has shown numerous biological activities, including anti-apoptotic, anti-inflammatory, and anti-atherosclerotic effects. The effect of PCA on traumatic brain injury (TBI)-induced neuronal death has not previously been evaluated. TBI is defined as damage to the brain resulting from external mechanical force, such as rapid acceleration or deceleration, impact, blast waves, or penetration by a projectile. TBI causes neuronal death in the hippocampus and cerebral cortex. The present study aimed to evaluate the therapeutic potential of PCA on TBI-induced neuronal death. Here, TBI was induced by a controlled cortical impact model using rats. PCA (30 mg/kg) was injected into the intraperitoneal (ip) space immediately after TBI. Neuronal death was evaluated with Fluoro Jade-B (FJB) staining at 24 h after TBI. Oxidative injury was detected by 4-hydroxy-2-nonenal (4HNE), glutathione (GSH) concentration was analyzed by glutathione adduct with N-ethylmaleimide (GS-NEM) staining at 24 h after TBI, and microglial activation in the hippocampus was detected by CD11b immunohistochemistry at one week after TBI. We found that the proportion of degenerating neurons, oxidative injury, GSH depletion, and microglia activation in the hippocampus and cortex were all reduced by PCA treatment following TBI. Therefore, our study suggests that PCA may have therapeutic potential in preventing TBI-induced neuronal death.
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spelling pubmed-57511132018-01-08 Administration of Protocatechuic Acid Reduces Traumatic Brain Injury-Induced Neuronal Death Lee, Sang Hwon Choi, Bo Young Lee, Song Hee Kho, A. Ra Jeong, Jeong Hyun Hong, Dae Ki Suh, Sang Won Int J Mol Sci Article Protocatechuic acid (PCA) was first purified from green tea and has shown numerous biological activities, including anti-apoptotic, anti-inflammatory, and anti-atherosclerotic effects. The effect of PCA on traumatic brain injury (TBI)-induced neuronal death has not previously been evaluated. TBI is defined as damage to the brain resulting from external mechanical force, such as rapid acceleration or deceleration, impact, blast waves, or penetration by a projectile. TBI causes neuronal death in the hippocampus and cerebral cortex. The present study aimed to evaluate the therapeutic potential of PCA on TBI-induced neuronal death. Here, TBI was induced by a controlled cortical impact model using rats. PCA (30 mg/kg) was injected into the intraperitoneal (ip) space immediately after TBI. Neuronal death was evaluated with Fluoro Jade-B (FJB) staining at 24 h after TBI. Oxidative injury was detected by 4-hydroxy-2-nonenal (4HNE), glutathione (GSH) concentration was analyzed by glutathione adduct with N-ethylmaleimide (GS-NEM) staining at 24 h after TBI, and microglial activation in the hippocampus was detected by CD11b immunohistochemistry at one week after TBI. We found that the proportion of degenerating neurons, oxidative injury, GSH depletion, and microglia activation in the hippocampus and cortex were all reduced by PCA treatment following TBI. Therefore, our study suggests that PCA may have therapeutic potential in preventing TBI-induced neuronal death. MDPI 2017-11-23 /pmc/articles/PMC5751113/ /pubmed/29168791 http://dx.doi.org/10.3390/ijms18122510 Text en © 2017 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Lee, Sang Hwon
Choi, Bo Young
Lee, Song Hee
Kho, A. Ra
Jeong, Jeong Hyun
Hong, Dae Ki
Suh, Sang Won
Administration of Protocatechuic Acid Reduces Traumatic Brain Injury-Induced Neuronal Death
title Administration of Protocatechuic Acid Reduces Traumatic Brain Injury-Induced Neuronal Death
title_full Administration of Protocatechuic Acid Reduces Traumatic Brain Injury-Induced Neuronal Death
title_fullStr Administration of Protocatechuic Acid Reduces Traumatic Brain Injury-Induced Neuronal Death
title_full_unstemmed Administration of Protocatechuic Acid Reduces Traumatic Brain Injury-Induced Neuronal Death
title_short Administration of Protocatechuic Acid Reduces Traumatic Brain Injury-Induced Neuronal Death
title_sort administration of protocatechuic acid reduces traumatic brain injury-induced neuronal death
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5751113/
https://www.ncbi.nlm.nih.gov/pubmed/29168791
http://dx.doi.org/10.3390/ijms18122510
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