title: Snailase preparation of ginsenoside M1 from protopanaxadiol-type ginsenoside and their protective effects against CCl4-induced chronic hepatotoxicity in mice.
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.
authors.affiliation: Norman Bethune College of Medicine, Jilin University, Changchun 130021, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Li
authors.forename: Ming
authors.initials: M
authors.lastname: Zhang
authors.forename: Yi-Nan
authors.initials: YN
authors.lastname: Zheng
authors.forename: Jing
authors.initials: J
authors.lastname: Li
authors.forename: Ying-Ping
authors.initials: YP
authors.lastname: Wang
authors.forename: Yun-Jing
authors.initials: YJ
authors.lastname: Wang
authors.forename: Jian
authors.initials: J
authors.lastname: Gu
authors.forename: Ying
authors.initials: Y
authors.lastname: Jin
authors.forename: Hui
authors.initials: H
authors.lastname: Wang
authors.forename: Li
authors.initials: L
authors.lastname: Chen
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001219:Aspartate Aminotransferases / Q000097:blood; D001711:Biotransformation / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D002251:Carbon Tetrachloride; D056486:Chemical and Drug Induced Liver Injury / Q000097:blood / Q000188:drug therapy* / Q000473:pathology; D002851:Chromatography, High Pressure Liquid; D002908:Chronic Disease; D036145:Ginsenosides / Q000737:chemistry / Q000494:pharmacology / Q000627:therapeutic use*; D008099:Liver / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D051379:Mice; D008813:Mice, Inbred ICR; D009929:Organ Size / Q000187:drug effects; D020011:Protective Agents / Q000737:chemistry / Q000494:pharmacology / Q000627:therapeutic use*; D012502:Sapogenins / Q000737:chemistry / Q000494:pharmacology / Q000627:therapeutic use*; D012908:Snails / Q000201:enzymology*; D021241:Spectrometry, Mass, Electrospray Ionization; D013482:Superoxide Dismutase / Q000378:metabolism; D014020:Tissue Extracts
chemical_list: D000410:Alanine Transaminase; D000975:Antioxidants; D001219:Aspartate Aminotransferases; D002251:Carbon Tetrachloride; D036145:Ginsenosides; D008315:Malondialdehyde; D020011:Protective Agents; D012502:Sapogenins; D013482:Superoxide Dismutase; D014020:Tissue Extracts; C112772:ginsenoside compound K; C062916:protopanaxadiol