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Protective Effect of Korean Red Ginseng against Aflatoxin B(1)-Induced Hepatotoxicity in Rat
Korean red ginseng (KRG), the steamed root of Panax ginseng Meyer, has a variety of biological properties, including anti-inflammatory, antioxidant and anticancer effects. Aflatoxin B(1) (AFB(1)) produced by the Aspergillus spp. causes acute hepatotoxicity by lipid peroxidation and oxidative DNA dam...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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The Korean Society of Ginseng
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3659521/ https://www.ncbi.nlm.nih.gov/pubmed/23717067 http://dx.doi.org/10.5142/jgr.2011.35.2.243 |
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author | Kim, Yong-Seong Kim, Yong-Hoon Noh, Jung-Ran Cho, Eun-Sang Park, Jong-Ho Son, Hwa-Young |
author_facet | Kim, Yong-Seong Kim, Yong-Hoon Noh, Jung-Ran Cho, Eun-Sang Park, Jong-Ho Son, Hwa-Young |
author_sort | Kim, Yong-Seong |
collection | PubMed |
description | Korean red ginseng (KRG), the steamed root of Panax ginseng Meyer, has a variety of biological properties, including anti-inflammatory, antioxidant and anticancer effects. Aflatoxin B(1) (AFB(1)) produced by the Aspergillus spp. causes acute hepatotoxicity by lipid peroxidation and oxidative DNA damage, and induces liver carcinoma in humans and laboratory animals. This study was performed to examine the protective effects of KRG against hepatotoxicity induced by AFB(1) using liver-specific serum marker analysis, histopathology, and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling. In addition, to elucidate the possible mechanism of hepatoprotective effects, superoxide dismutase, catalase, glutathione peroxidase, and malondialdehyde were analyzed. Rats were treated with 250 mg/kg of KRG (KRG group) or saline (AFB(1) group) for 4 weeks and then received 150 μg/kg of AFB(1) intraperitoneally for 3 days. Rats were sacrificed at 12 h, 24 h, 48 h, 72 h, or 1 wk after AFB(1) treatment. In the KRG pre-treatment group, serum alanine aminotransferase, aspartate aminotransferase, and malondialdehyde levels were low, but superoxide dismutase, catalase, and glutathione peroxidase activities were high as compared to the AFB(1) alone group. Histopathologically, AFB(1) treatment induced necrosis and apoptosis in hepatocytes, and led to inflammatory cells infiltration in the liver. KRG pre-treatment ameliorated these changes. These results indicate that KRG may have protective effects against hepatotoxicity induced by AFB(1) that involve the antioxidant properties of KRG. |
format | Online Article Text |
id | pubmed-3659521 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | The Korean Society of Ginseng |
record_format | MEDLINE/PubMed |
spelling | pubmed-36595212013-05-28 Protective Effect of Korean Red Ginseng against Aflatoxin B(1)-Induced Hepatotoxicity in Rat Kim, Yong-Seong Kim, Yong-Hoon Noh, Jung-Ran Cho, Eun-Sang Park, Jong-Ho Son, Hwa-Young J Ginseng Res Articles Korean red ginseng (KRG), the steamed root of Panax ginseng Meyer, has a variety of biological properties, including anti-inflammatory, antioxidant and anticancer effects. Aflatoxin B(1) (AFB(1)) produced by the Aspergillus spp. causes acute hepatotoxicity by lipid peroxidation and oxidative DNA damage, and induces liver carcinoma in humans and laboratory animals. This study was performed to examine the protective effects of KRG against hepatotoxicity induced by AFB(1) using liver-specific serum marker analysis, histopathology, and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling. In addition, to elucidate the possible mechanism of hepatoprotective effects, superoxide dismutase, catalase, glutathione peroxidase, and malondialdehyde were analyzed. Rats were treated with 250 mg/kg of KRG (KRG group) or saline (AFB(1) group) for 4 weeks and then received 150 μg/kg of AFB(1) intraperitoneally for 3 days. Rats were sacrificed at 12 h, 24 h, 48 h, 72 h, or 1 wk after AFB(1) treatment. In the KRG pre-treatment group, serum alanine aminotransferase, aspartate aminotransferase, and malondialdehyde levels were low, but superoxide dismutase, catalase, and glutathione peroxidase activities were high as compared to the AFB(1) alone group. Histopathologically, AFB(1) treatment induced necrosis and apoptosis in hepatocytes, and led to inflammatory cells infiltration in the liver. KRG pre-treatment ameliorated these changes. These results indicate that KRG may have protective effects against hepatotoxicity induced by AFB(1) that involve the antioxidant properties of KRG. The Korean Society of Ginseng 2011-06 /pmc/articles/PMC3659521/ /pubmed/23717067 http://dx.doi.org/10.5142/jgr.2011.35.2.243 Text en Copyright ©2011, 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 Kim, Yong-Seong Kim, Yong-Hoon Noh, Jung-Ran Cho, Eun-Sang Park, Jong-Ho Son, Hwa-Young Protective Effect of Korean Red Ginseng against Aflatoxin B(1)-Induced Hepatotoxicity in Rat |
title | Protective Effect of Korean Red Ginseng against Aflatoxin B(1)-Induced Hepatotoxicity in Rat |
title_full | Protective Effect of Korean Red Ginseng against Aflatoxin B(1)-Induced Hepatotoxicity in Rat |
title_fullStr | Protective Effect of Korean Red Ginseng against Aflatoxin B(1)-Induced Hepatotoxicity in Rat |
title_full_unstemmed | Protective Effect of Korean Red Ginseng against Aflatoxin B(1)-Induced Hepatotoxicity in Rat |
title_short | Protective Effect of Korean Red Ginseng against Aflatoxin B(1)-Induced Hepatotoxicity in Rat |
title_sort | protective effect of korean red ginseng against aflatoxin b(1)-induced hepatotoxicity in rat |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3659521/ https://www.ncbi.nlm.nih.gov/pubmed/23717067 http://dx.doi.org/10.5142/jgr.2011.35.2.243 |
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