ArticleMolecules (Basel, Switzerland)2011
Snailase preparation of ginsenoside M1 from protopanaxadiol-type ginsenoside and their protective effects against CCl4-induced chronic hepatotoxicity in mice.
Article in Molecules (Basel, Switzerland), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 22 citations in OpenAlex.
- The effect of ginsenosides on liver injury in preclinical studies: a systematic review and meta-analysis.Frontiers in pharmacology · 2023Review
- Ginsenoside Compound K: Insights into Recent Studies on Pharmacokinetics and Health-Promoting Activities.Biomolecules · 2020Review
- Microbial conversion of major ginsenosides in ginseng total saponins byJournal of ginseng research · 2016Article
- Role of the Red Ginseng in Defense against the Environmental Heat Stress in Sprague Dawley Rats.Molecules (Basel, Switzerland) · 2015Article
- Article
- Highly efficient biotransformation of polydatin to resveratrol by snailase hydrolysis using response surface methodology optimization.Molecules (Basel, Switzerland) · 2013Article
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Authors and funding
10 authors at 4 institutions in 1 country.
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Abstract
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.
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