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Snailase Preparation of Ginsenoside M1 from Protopanaxadiol-Type Ginsenoside and Their Protective Effects Against CCl(4)-Induced Chronic Hepatotoxicity in Mice
To investigate the protective effects of protopanaxadiol-type ginsenoside (PDG) and its metabolite ginsenoside M1 (G-M1) on carbon tetrachloride (CCl(4))-induced chronic liver injury in ICR mice, we carried out conversion of protopanaxadiol-type ginsenosides to ginsenoside M1 using snailase. The opt...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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MDPI
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6264268/ https://www.ncbi.nlm.nih.gov/pubmed/22146371 http://dx.doi.org/10.3390/molecules161210093 |
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author | Li, Wei Zhang, Ming Zheng, Yi-Nan Li, Jing Wang, Ying-Ping Wang, Yun-Jing Gu, Jian Jin, Ying Wang, Hui Chen, Li |
author_facet | Li, Wei Zhang, Ming Zheng, Yi-Nan Li, Jing Wang, Ying-Ping Wang, Yun-Jing Gu, Jian Jin, Ying Wang, Hui Chen, Li |
author_sort | Li, Wei |
collection | PubMed |
description | To investigate the protective effects of protopanaxadiol-type ginsenoside (PDG) and its metabolite ginsenoside M1 (G-M1) on carbon tetrachloride (CCl(4))-induced chronic liver injury in ICR mice, we carried out conversion of protopanaxadiol-type ginsenosides to ginsenoside M1 using snailase. The optimum time for the conversion was 24 h at a constant pH of 4.5 and an optimum temperature of 50 °C. The transformation products were identified by high-performance liquid chromatography and electrospray ion-mass spectrometry. Subsequently, most of PDG was decomposed and converted into G-M1 by 24 h post-reaction. During the study on hepatoprotective in a mice model of chronic liver injury, PDG or G-M1 supplement significantly ameliorated the CCl(4)-induced liver lesions, lowered the serum levels of select hepatic enzyme markers (alanine aminotransferase, ALT, and aspartate aminotransferase, AST) and malondialdehyde and increased the activity of superoxide dismutase in liver. Histopathology of the liver tissues showed that PDG and G-M1 attenuated the hepatocellular necrosis and led to reduction of inflammatory cell infiltration. Therefore, the results of this study show that PDG and G-M1 can be proposed to protect the liver against CCl(4)-induced oxidative injury in mice, and the hepatoprotective effect might be attributed to amelioration of oxidative stress. |
format | Online Article Text |
id | pubmed-6264268 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-62642682018-12-10 Snailase Preparation of Ginsenoside M1 from Protopanaxadiol-Type Ginsenoside and Their Protective Effects Against CCl(4)-Induced Chronic Hepatotoxicity in Mice Li, Wei Zhang, Ming Zheng, Yi-Nan Li, Jing Wang, Ying-Ping Wang, Yun-Jing Gu, Jian Jin, Ying Wang, Hui Chen, Li Molecules Article To investigate the protective effects of protopanaxadiol-type ginsenoside (PDG) and its metabolite ginsenoside M1 (G-M1) on carbon tetrachloride (CCl(4))-induced chronic liver injury in ICR mice, we carried out conversion of protopanaxadiol-type ginsenosides to ginsenoside M1 using snailase. The optimum time for the conversion was 24 h at a constant pH of 4.5 and an optimum temperature of 50 °C. The transformation products were identified by high-performance liquid chromatography and electrospray ion-mass spectrometry. Subsequently, most of PDG was decomposed and converted into G-M1 by 24 h post-reaction. During the study on hepatoprotective in a mice model of chronic liver injury, PDG or G-M1 supplement significantly ameliorated the CCl(4)-induced liver lesions, lowered the serum levels of select hepatic enzyme markers (alanine aminotransferase, ALT, and aspartate aminotransferase, AST) and malondialdehyde and increased the activity of superoxide dismutase in liver. Histopathology of the liver tissues showed that PDG and G-M1 attenuated the hepatocellular necrosis and led to reduction of inflammatory cell infiltration. Therefore, the results of this study show that PDG and G-M1 can be proposed to protect the liver against CCl(4)-induced oxidative injury in mice, and the hepatoprotective effect might be attributed to amelioration of oxidative stress. MDPI 2011-12-06 /pmc/articles/PMC6264268/ /pubmed/22146371 http://dx.doi.org/10.3390/molecules161210093 Text en © 2011 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 license (http://creativecommons.org/licenses/by/3.0/). |
spellingShingle | Article Li, Wei Zhang, Ming Zheng, Yi-Nan Li, Jing Wang, Ying-Ping Wang, Yun-Jing Gu, Jian Jin, Ying Wang, Hui Chen, Li Snailase Preparation of Ginsenoside M1 from Protopanaxadiol-Type Ginsenoside and Their Protective Effects Against CCl(4)-Induced Chronic Hepatotoxicity in Mice |
title | Snailase Preparation of Ginsenoside M1 from Protopanaxadiol-Type Ginsenoside and Their Protective Effects Against CCl(4)-Induced Chronic Hepatotoxicity in Mice |
title_full | Snailase Preparation of Ginsenoside M1 from Protopanaxadiol-Type Ginsenoside and Their Protective Effects Against CCl(4)-Induced Chronic Hepatotoxicity in Mice |
title_fullStr | Snailase Preparation of Ginsenoside M1 from Protopanaxadiol-Type Ginsenoside and Their Protective Effects Against CCl(4)-Induced Chronic Hepatotoxicity in Mice |
title_full_unstemmed | Snailase Preparation of Ginsenoside M1 from Protopanaxadiol-Type Ginsenoside and Their Protective Effects Against CCl(4)-Induced Chronic Hepatotoxicity in Mice |
title_short | Snailase Preparation of Ginsenoside M1 from Protopanaxadiol-Type Ginsenoside and Their Protective Effects Against CCl(4)-Induced Chronic Hepatotoxicity in Mice |
title_sort | snailase preparation of ginsenoside m1 from protopanaxadiol-type ginsenoside and their protective effects against ccl(4)-induced chronic hepatotoxicity in mice |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6264268/ https://www.ncbi.nlm.nih.gov/pubmed/22146371 http://dx.doi.org/10.3390/molecules161210093 |
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