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Protective Effects of the Key Compounds Isolated from Corni fructus against β-Amyloid-Induced Neurotoxicity in PC12 Cells
β-Amyloid (Aβ) peptide is the major component of senile plaques and is considered to have a causal role in the development and progression of Alzheimer’s disease (AD). There is compelling evidence supporting the notion that Aβ-induced cytotoxicity is mediated though the generation of ROS. In the pre...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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MDPI
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6268534/ https://www.ncbi.nlm.nih.gov/pubmed/22964500 http://dx.doi.org/10.3390/molecules170910831 |
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author | Hong, Seung-Young Jeong, Woo-Sik Jun, Mira |
author_facet | Hong, Seung-Young Jeong, Woo-Sik Jun, Mira |
author_sort | Hong, Seung-Young |
collection | PubMed |
description | β-Amyloid (Aβ) peptide is the major component of senile plaques and is considered to have a causal role in the development and progression of Alzheimer’s disease (AD). There is compelling evidence supporting the notion that Aβ-induced cytotoxicity is mediated though the generation of ROS. In the present study, we investigated the neuroprotective effects of ursolic acid (UA), p-coumaric acid (p-CA), and gallic acid (GA) isolated from Corni fructus (CF) against Aβ(25–35)-induced toxicity in PC12 cell. Exposure of PC12 cells to 50 μM Aβ(25–35) increased cellular oxidative stress, the number of apoptotic cells and caspase-3 activity and finally caused significant cell death. However, UA, p-CA, and GA not only suppressed the generation of ROS but also attenuated DNA fragmentation and eventually attenuated Aβ-induced apoptosis in a dose-dependent manner. In protecting cells against Aβ neurotoxicity, UA and GA possessed stronger ability against ROS generation than p-CA, while p-CA showed the strongest anti-apoptotic activity. Particularly, p-CA protected cells at the concentration range from 0.5 up to 125 μM without any adverse effect. Taken together, these effects of UA, p-CA, and GA may be partly associated with the neuroprotective effect of CF. Furthermore, our findings might raise a possibility of therapeutic applications of CF for preventing and/or treating neurodegenerative diseases. |
format | Online Article Text |
id | pubmed-6268534 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-62685342018-12-12 Protective Effects of the Key Compounds Isolated from Corni fructus against β-Amyloid-Induced Neurotoxicity in PC12 Cells Hong, Seung-Young Jeong, Woo-Sik Jun, Mira Molecules Article β-Amyloid (Aβ) peptide is the major component of senile plaques and is considered to have a causal role in the development and progression of Alzheimer’s disease (AD). There is compelling evidence supporting the notion that Aβ-induced cytotoxicity is mediated though the generation of ROS. In the present study, we investigated the neuroprotective effects of ursolic acid (UA), p-coumaric acid (p-CA), and gallic acid (GA) isolated from Corni fructus (CF) against Aβ(25–35)-induced toxicity in PC12 cell. Exposure of PC12 cells to 50 μM Aβ(25–35) increased cellular oxidative stress, the number of apoptotic cells and caspase-3 activity and finally caused significant cell death. However, UA, p-CA, and GA not only suppressed the generation of ROS but also attenuated DNA fragmentation and eventually attenuated Aβ-induced apoptosis in a dose-dependent manner. In protecting cells against Aβ neurotoxicity, UA and GA possessed stronger ability against ROS generation than p-CA, while p-CA showed the strongest anti-apoptotic activity. Particularly, p-CA protected cells at the concentration range from 0.5 up to 125 μM without any adverse effect. Taken together, these effects of UA, p-CA, and GA may be partly associated with the neuroprotective effect of CF. Furthermore, our findings might raise a possibility of therapeutic applications of CF for preventing and/or treating neurodegenerative diseases. MDPI 2012-09-10 /pmc/articles/PMC6268534/ /pubmed/22964500 http://dx.doi.org/10.3390/molecules170910831 Text en © 2012 by the authors; licensee MDPI, Basel, Switzerland. http://creativecommons.org/licenses/by/3.0/ This article is an open-access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/). |
spellingShingle | Article Hong, Seung-Young Jeong, Woo-Sik Jun, Mira Protective Effects of the Key Compounds Isolated from Corni fructus against β-Amyloid-Induced Neurotoxicity in PC12 Cells |
title | Protective Effects of the Key Compounds Isolated from Corni fructus against β-Amyloid-Induced Neurotoxicity in PC12 Cells |
title_full | Protective Effects of the Key Compounds Isolated from Corni fructus against β-Amyloid-Induced Neurotoxicity in PC12 Cells |
title_fullStr | Protective Effects of the Key Compounds Isolated from Corni fructus against β-Amyloid-Induced Neurotoxicity in PC12 Cells |
title_full_unstemmed | Protective Effects of the Key Compounds Isolated from Corni fructus against β-Amyloid-Induced Neurotoxicity in PC12 Cells |
title_short | Protective Effects of the Key Compounds Isolated from Corni fructus against β-Amyloid-Induced Neurotoxicity in PC12 Cells |
title_sort | protective effects of the key compounds isolated from corni fructus against β-amyloid-induced neurotoxicity in pc12 cells |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6268534/ https://www.ncbi.nlm.nih.gov/pubmed/22964500 http://dx.doi.org/10.3390/molecules170910831 |
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