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Sun Ginseng Protects Endothelial Progenitor Cells From Senescence Associated Apoptosis
Endothelial progenitor cells (EPC) are a population of cells that circulate in the blood stream. They play a role in angiogenesis and, therefore, can be prognostic markers of vascular repair. Ginsenoside Rg(3) prevents endothelial cell apoptosis through the inhibition of the mitochondrial caspase pa...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Korean Society of Ginseng
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3659567/ https://www.ncbi.nlm.nih.gov/pubmed/23717107 http://dx.doi.org/10.5142/jgr.2012.36.1.78 |
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author | Im, Wooseok Chung, Jin-Young Bhan, Jaejun Lim, Jiyeon Lee, Soon-Tae Chu, Kon Kim, Manho |
author_facet | Im, Wooseok Chung, Jin-Young Bhan, Jaejun Lim, Jiyeon Lee, Soon-Tae Chu, Kon Kim, Manho |
author_sort | Im, Wooseok |
collection | PubMed |
description | Endothelial progenitor cells (EPC) are a population of cells that circulate in the blood stream. They play a role in angiogenesis and, therefore, can be prognostic markers of vascular repair. Ginsenoside Rg(3) prevents endothelial cell apoptosis through the inhibition of the mitochondrial caspase pathway. It also affects estrogen activity, which reduces EPC senescence. Sun ginseng (SG), which is heat-processed ginseng, has a high content of ginsenosides. The purpose of this study was to investigate the protective effects of SG on senescence-associated apoptosis in EPCs. In order to isolate EPCs, mononuclear cells of human blood buffy coats were cultured and characterized by their uptake of acetylated low-density lipoprotein (acLDL) and their binding of Ulex europaeus agglutinin I (ulex-lectin). Flow cytometry with annexin-V staining was performed in order to assess early and late apoptosis. Senescence was determined by β-galactosidase (β-gal) staining. Staining with 4′-6-Diamidino-2-phenylindole verified that most adherent cells (93±2.7%) were acLDL-positive and ulex-lectin-positive. The percentage of β-gal-positive EPCs was decreased from 93.8±2.0% to 62.5±3.6% by SG treatment. A fluorescence-activated cell sorter (FACS) analysis showed that 4.9% of EPCs were late apoptotic in controls. Sun ginseng decreased the apoptotic cell population by 39% in the late stage of apoptosis from control baseline levels. In conclusion, these results show antisenescent and antiapoptotic effects of SG in human-derived EPCs, indicating that SG can enhance EPC-mediated repair mechanisms. |
format | Online Article Text |
id | pubmed-3659567 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | The Korean Society of Ginseng |
record_format | MEDLINE/PubMed |
spelling | pubmed-36595672013-05-28 Sun Ginseng Protects Endothelial Progenitor Cells From Senescence Associated Apoptosis Im, Wooseok Chung, Jin-Young Bhan, Jaejun Lim, Jiyeon Lee, Soon-Tae Chu, Kon Kim, Manho J Ginseng Res Articles Endothelial progenitor cells (EPC) are a population of cells that circulate in the blood stream. They play a role in angiogenesis and, therefore, can be prognostic markers of vascular repair. Ginsenoside Rg(3) prevents endothelial cell apoptosis through the inhibition of the mitochondrial caspase pathway. It also affects estrogen activity, which reduces EPC senescence. Sun ginseng (SG), which is heat-processed ginseng, has a high content of ginsenosides. The purpose of this study was to investigate the protective effects of SG on senescence-associated apoptosis in EPCs. In order to isolate EPCs, mononuclear cells of human blood buffy coats were cultured and characterized by their uptake of acetylated low-density lipoprotein (acLDL) and their binding of Ulex europaeus agglutinin I (ulex-lectin). Flow cytometry with annexin-V staining was performed in order to assess early and late apoptosis. Senescence was determined by β-galactosidase (β-gal) staining. Staining with 4′-6-Diamidino-2-phenylindole verified that most adherent cells (93±2.7%) were acLDL-positive and ulex-lectin-positive. The percentage of β-gal-positive EPCs was decreased from 93.8±2.0% to 62.5±3.6% by SG treatment. A fluorescence-activated cell sorter (FACS) analysis showed that 4.9% of EPCs were late apoptotic in controls. Sun ginseng decreased the apoptotic cell population by 39% in the late stage of apoptosis from control baseline levels. In conclusion, these results show antisenescent and antiapoptotic effects of SG in human-derived EPCs, indicating that SG can enhance EPC-mediated repair mechanisms. The Korean Society of Ginseng 2012-01 /pmc/articles/PMC3659567/ /pubmed/23717107 http://dx.doi.org/10.5142/jgr.2012.36.1.78 Text en Copyright ©2012, The Korean Society of Ginseng http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Articles Im, Wooseok Chung, Jin-Young Bhan, Jaejun Lim, Jiyeon Lee, Soon-Tae Chu, Kon Kim, Manho Sun Ginseng Protects Endothelial Progenitor Cells From Senescence Associated Apoptosis |
title | Sun Ginseng Protects Endothelial Progenitor Cells From Senescence Associated Apoptosis |
title_full | Sun Ginseng Protects Endothelial Progenitor Cells From Senescence Associated Apoptosis |
title_fullStr | Sun Ginseng Protects Endothelial Progenitor Cells From Senescence Associated Apoptosis |
title_full_unstemmed | Sun Ginseng Protects Endothelial Progenitor Cells From Senescence Associated Apoptosis |
title_short | Sun Ginseng Protects Endothelial Progenitor Cells From Senescence Associated Apoptosis |
title_sort | sun ginseng protects endothelial progenitor cells from senescence associated apoptosis |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3659567/ https://www.ncbi.nlm.nih.gov/pubmed/23717107 http://dx.doi.org/10.5142/jgr.2012.36.1.78 |
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