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Effect of black garlic on acute alcohol‐induced hangover and chronic alcohol‐induced liver injury in rats
Author(s) -
Kim Min Hee,
Kim Mi Yeon,
Son Chan Wok,
Cheong Sun Hee,
Kim Mee Ree
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.111.6
Subject(s) - chemistry , aspartate transaminase , glutathione reductase , lipid peroxidation , glutathione peroxidase , glutathione , alanine transaminase , acetaldehyde , cyp2e1 , pharmacology , liver injury , biochemistry , antioxidant , catalase , ethanol , medicine , alkaline phosphatase , enzyme , microsome
The hepatoprotective effect of black garlic against ethanol‐induced oxidative damage was investigated in adult male SD rats. Black garlic (50, 100 and 400mg/kg) and ethanol (15mL/kg, 20% w/v) were administered orally to animals for 4 weeks. To investigate anti‐hangover effect, alcohol and acetaldehyde concentration of blood were measured at 1, 3, 5 and 7 h after oral black garlic and ethanol treatment. Blood alcohol and acetaldehyde concentration were dose‐dependently reduced in BG compared to ET. Serum alanine transaminase, aspartate transaminase, alkaline phosphatase, lactate dehydrogenase activities of BG were significantly decreased compared to those of ET. Lipid peroxidations of BG were significantly decreased in blood, liver, heart and kidney, compared to those of ET. Glutathione content in liver and RBC, antioxidant and anticancer enzyme activities such as glutathione peroxidase, glutathione reductase, catalase, quinone reductase and glutathione‐S‐transferase were improved in rats administered black garlic. The pretreatment of black garlic also significantly decreased by 45% in cytochrome P450 2E1 (CYP2E1) activity as well as lymphocyte DND damage expressed by tail length using the comet assay. These results support that the pretreatment of black garlic could provide preventive effect against alcohol‐induced liver injury through suppression of lipid peroxidation and oxidative DNA damage.