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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...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2017
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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. |
format | Online Article Text |
id | pubmed-5751113 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
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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