PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 31735662-7 2019 RESULTS: The results showed that propofol significantly prevented d-GalN/LPS-induced liver damage by preventing associated increases of serum alanine transaminase (ALT) and aspartate transaminase (AST) and restoring liver histopathological changes. Galactosamine 66-72 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 197-200 24554039-6 2014 Results showed that GalN/LPS induced marked elevations in serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT). Galactosamine 20-24 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 64-90 31637892-7 2019 RESULTS: SEB induced liver injury in D-galactosamine (D-gal)-sensitized mice, as demonstrated by increased serum levels of AST and ALT, elevated release of interferon-gamma (INF-gamma), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and IL-2, and promoted infiltrating immune cells into liver. Galactosamine 37-52 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 123-126 24472388-4 2014 injection of GalN (500 mg/kg body weight) in mice treated with bovine serum albumin (BSA) for 14 d significantly increased serum aspartate aminotransferase (AST) concentrations compared with the untreated mice. Galactosamine 13-17 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 157-160 31814922-4 2019 RESULTS: GalN/LPS produced acute hepatic injury by a sharp increase in serum AST, ALT, and TNF-alpha levels, increases that were ameliorated in the experimental groups. Galactosamine 9-13 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 77-80 25706292-4 2015 Injection of SEB into D-galactosamine-sensitized female C57BL/6 mice resulted in liver injury as indicated by an increase in enzyme aspartate transaminase (AST) levels, induction of inflammatory cytokines, and massive infiltration of immune cells into the liver. Galactosamine 22-37 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 132-154 25706292-4 2015 Injection of SEB into D-galactosamine-sensitized female C57BL/6 mice resulted in liver injury as indicated by an increase in enzyme aspartate transaminase (AST) levels, induction of inflammatory cytokines, and massive infiltration of immune cells into the liver. Galactosamine 22-37 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 156-159 24472388-4 2014 injection of GalN (500 mg/kg body weight) in mice treated with bovine serum albumin (BSA) for 14 d significantly increased serum aspartate aminotransferase (AST) concentrations compared with the untreated mice. Galactosamine 13-17 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 129-155 24554039-6 2014 Results showed that GalN/LPS induced marked elevations in serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT). Galactosamine 20-24 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 92-95 15742813-5 2005 Ten of the synthesized chalcone derivatives exhibited inhibitory effects on D-GalN/LPS-induced levels of AST and ALT in mice. Galactosamine 76-82 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 105-108 17420605-2 2007 CS significantly suppressed the GalN-induced elevation of ALT and AST activities. Galactosamine 32-36 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 66-69 17420605-3 2007 Each of four concentrated fractions extracted from sake (respectively consisting mainly of basic amino acids, neutral and acidic amino acids, organic acids and sugars) suppressed the GalN-induced elevation of ALT and AST activities. Galactosamine 183-187 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 217-220 17420605-4 2007 We focused on the sugar fraction containing glucose and ethyl alpha-D-glucoside (alpha-EG), which is a sake-specific sugar, as the major components and demonstrated that only alpha-EG showed significant suppression of the GalN-induced elevation of ALT and AST activities. Galactosamine 222-226 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 256-259 16619363-4 2006 All the mice injected with LPS and GalN (control group) died of histopathologically congestive and hemorrhagic hepatic insufficiency within 24 h, showing significantly increased activities of plasma aspartate aminotransferase (AST; 380 IU/mL) and alanine aminotransferase (ALT; 130 IU/mL). Galactosamine 35-39 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 199-225 19282658-7 2009 Bach1-deficiency suppressed induction of plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities in response to the GalN/LPS-treatment. Galactosamine 146-150 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 83-109 19282658-7 2009 Bach1-deficiency suppressed induction of plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities in response to the GalN/LPS-treatment. Galactosamine 146-150 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 111-114 18670093-4 2008 The activities of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in mice indicated the highest peaks at 12 h after D-GalN/LPS injection, then the activities of serum ALT and AST rapidly decreased. Galactosamine 142-148 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 59-85 18670093-4 2008 The activities of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in mice indicated the highest peaks at 12 h after D-GalN/LPS injection, then the activities of serum ALT and AST rapidly decreased. Galactosamine 142-148 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 87-90 16619363-4 2006 All the mice injected with LPS and GalN (control group) died of histopathologically congestive and hemorrhagic hepatic insufficiency within 24 h, showing significantly increased activities of plasma aspartate aminotransferase (AST; 380 IU/mL) and alanine aminotransferase (ALT; 130 IU/mL). Galactosamine 35-39 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 227-230 16051691-2 2005 The numbers of necrotic and apoptotic hepatocytes in the liver, as well as the levels of serum aspartate transaminase (AST) and alanine transaminase (ALT), were increased significantly by GalN/LPS treatment compared to the appropriate controls. Galactosamine 188-192 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 95-117 16051691-2 2005 The numbers of necrotic and apoptotic hepatocytes in the liver, as well as the levels of serum aspartate transaminase (AST) and alanine transaminase (ALT), were increased significantly by GalN/LPS treatment compared to the appropriate controls. Galactosamine 188-192 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 119-122 15852491-2 2005 Co-administration of D-GalN (700 mg[sol ]kg) and LPS (1 microg[sol ]kg) significantly (p < 0.05) raised the plasma levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in mice in the toxin group compared with the values in the control group. Galactosamine 21-27 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 163-189 15852491-2 2005 Co-administration of D-GalN (700 mg[sol ]kg) and LPS (1 microg[sol ]kg) significantly (p < 0.05) raised the plasma levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in mice in the toxin group compared with the values in the control group. Galactosamine 21-27 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 191-194 15239101-4 2004 GalN/LPS treatment induced significant increases in aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels in the blood, apoptotic and necrotic changes in hepatocytes, and/or showed a high degree of lethality. Galactosamine 0-4 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 52-78 15239101-4 2004 GalN/LPS treatment induced significant increases in aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels in the blood, apoptotic and necrotic changes in hepatocytes, and/or showed a high degree of lethality. Galactosamine 0-4 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 80-83 15239101-6 2004 Pretreatment with adiponectin ameliorated the GalN/LPS-induced elevation of serum AST and ALT levels and the apoptotic and necrotic changes in hepatocytes, resulting in a reduction in lethality. Galactosamine 46-50 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 82-85