title: CGX, a traditional Korean medicine ameliorates concanavalin A-induced acute liver injury.
abstract: Concanavalin A (Con A)-induced acute liver injury model is well established as a model of T cell-mediated liver injury, in which T cells and NKT cells exert their cytotoxicity towards liver cells. In this study, we investigated the protective effects of CGX, a traditional Korean medicine against Con A-induced liver injury and its underlying mechanisms. After pretreatment with CGX (po, 50, 100 or 200 mg/kg) or distilled water once daily during 7 days, Con A (15 mg/kg) was injected intravenously. Thereafter serum level of AST and ALT, lipid peroxidation and cytokines in the liver tissue, and immune cell population in blood and the spleen were analyzed. CGX treatment reduced serum ALT, AST level in a dose-dependent manner. CGX treatment significantly decreased the lipid peroxidation and glutathione depletion in the liver tissue, and also lowered tissue levels of tumor necrotic factor-α and interferon-γ. CGX treatment attenuated the compositional alteration of Tc, Th, NKT, and B cells in blood as well as in the spleen. These results suggest that CGX has hepatoprotective property against Con A-induced liver injury through antioxidant action and immune regulation.
authors.affiliation: Liver and Immunology Research Center, Institute of Traditional Medicine and Bioscience of Daejeon University, Jung-gu, Daejeon, Republic of Korea.
authors.forename: Jang Woo
authors.initials: JW
authors.lastname: Shin
authors.forename: Jing Hua
authors.initials: JH
authors.lastname: Wang
authors.forename: Hyeong Geug
authors.initials: HG
authors.lastname: Kim
authors.forename: Hye Jung
authors.initials: HJ
authors.lastname: Park
authors.forename: Hee Sung
authors.initials: HS
authors.lastname: Bok
authors.forename: Chang Gue
authors.initials: CG
authors.lastname: Son
mesh_terms: D000818:Animals; D001835:Body Weight / Q000187:drug effects; D002374:Catalase / Q000378:metabolism; D056486:Chemical and Drug Induced Liver Injury / Q000473:pathology / Q000517:prevention & control*; D002851:Chromatography, High Pressure Liquid; D003208:Concanavalin A / Q000037:antagonists & inhibitors* / Q000633:toxicity*; D005978:Glutathione / Q000378:metabolism; D018836:Inflammation Mediators / Q000378:metabolism; D007371:Interferon-gamma / Q000378:metabolism; D008099:Liver / Q000737:chemistry / Q000201:enzymology / Q000473:pathology; D008111:Liver Function Tests; D016131:Lymphocyte Subsets / Q000187:drug effects; D008297:Male; D008315:Malondialdehyde / Q000032:analysis / Q000378:metabolism; D013058:Mass Spectrometry; D055670:Medicine, Korean Traditional; D051379:Mice; D008807:Mice, Inbred BALB C; D009929:Organ Size / Q000187:drug effects; D010449:Peptide Mapping; D010936:Plant Extracts / Q000494:pharmacology*; D013154:Spleen / Q000737:chemistry / Q000473:pathology; D013950:Thymus Gland / Q000737:chemistry / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D018836:Inflammation Mediators; D010936:Plant Extracts; D014409:Tumor Necrosis Factor-alpha; D003208:Concanavalin A; D008315:Malondialdehyde; D007371:Interferon-gamma; D002374:Catalase; D005978:Glutathione