PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 29619419-3 2018 To address this question, high-fat diet-fed mice were repeatedly administered D-galactosamine, which increases the sensitivity of hepatocytes to TNF-alpha-mediated apoptosis. Galactosamine 78-93 tumor necrosis factor Mus musculus 145-154 33760163-10 2021 In conclusion, the findings of the present study suggested that in a D-GalN/LPS-induced ALF model, TNF-alpha and IL-6 signaling may increase MLCK and ROCK expression levels, further mediate phosphorylation of MLC, which may result in tight junction dysregulation and intestinal barrier dysfunction. Galactosamine 69-75 tumor necrosis factor Mus musculus 99-108 33496031-5 2021 In vivo experiments in analbuminemic mice showed that these mice exhibit a more pronounced response to a model of TNFalpha-mediated liver injury induced by the administration of lipopolysaccharide (LPS) and D-galactosamine (D-gal). Galactosamine 207-222 tumor necrosis factor Mus musculus 114-122 33396223-5 2020 RESULTS: LPS/GalN injection generate distinct molecular processes, which includes increased production of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6), thus causing apoptosis as evident by increased caspase-3 activity. Galactosamine 13-17 tumor necrosis factor Mus musculus 106-133 33396223-5 2020 RESULTS: LPS/GalN injection generate distinct molecular processes, which includes increased production of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6), thus causing apoptosis as evident by increased caspase-3 activity. Galactosamine 13-17 tumor necrosis factor Mus musculus 135-144 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 tumor necrosis factor Mus musculus 91-100 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 tumor necrosis factor Mus musculus 186-213 31713877-9 2020 In addition, cilostazol was found to attenuate the TNF-stimulated phosphorylation of mitogen activated protein kinase (MAPK) and nuclear factor kappa-light-chain-enhancer of activated B cell (NF-kappaB) p65 in the aortic vascular smooth muscle cell line, MOVAS-1 and the D-gal plus TNF-challenged heart tissue of mouse. Galactosamine 271-276 tumor necrosis factor Mus musculus 51-54 30597306-5 2019 Moreover, AGD significantly inhibited LPS/GalN-induced inflammatory responses in mice with ALI by reducing not only the secretion of tumour necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6 but also the protein expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Galactosamine 42-46 tumor necrosis factor Mus musculus 133-167 29619419-4 2018 In mice treated with a high-fat diet plus D-galactosamine, hepatocyte apoptosis and liver fibrosis were induced, whereas both apoptosis and fibrosis were inhibited in these mice following gut sterilization with antimicrobials or knockout of TNF-alpha. Galactosamine 42-57 tumor necrosis factor Mus musculus 241-250 28125915-6 2018 Furthermore, GalN/LPS increased nuclear factor kappa-B activation and the levels of tumor necrosis factor-alpha and interleukin-1beta. Galactosamine 13-17 tumor necrosis factor Mus musculus 84-111 28822324-1 2017 Lipopolysaccharide/d-Galactosamine (LPS/d-Gal)-induced acute liver injury is characterized by significant inflammatory responses including TNF-alpha and interleukin-6 (IL-6) and is a widely applied experimental model for inflammation research. Galactosamine 19-34 tumor necrosis factor Mus musculus 139-148 28628850-1 2017 BACKGROUND: Exposure of mice to D-galactosamine (GalN) and lipopolysaccharide (LPS) induces acute liver failure through elevation of TNF-alpha, which causes liver damage resembling that in humans. Galactosamine 32-47 tumor necrosis factor Mus musculus 133-142 26141869-1 2015 BACKGROUND: Lipopolysaccharide/d-galactosamine (LPS/GalN)-induced hepatic injury is an experimental model of fulminant hepatic failure in which tumor necrosis factor alpha (TNF-alpha) plays a pivotal role. Galactosamine 31-46 tumor necrosis factor Mus musculus 144-171 28659918-7 2017 We further show that in the d-galactosamine (d-galN)/LPS-dependent lethality model, intraperitoneal injection of GBZ promoted mice survival, prevented liver damage, increased IL-10 levels, and inhibited TNF-alpha production. Galactosamine 28-43 tumor necrosis factor Mus musculus 203-212 26267221-0 2016 Kupffer-cell-expressed transmembrane TNF-alpha is a major contributor to lipopolysaccharide and D-galactosamine-induced liver injury. Galactosamine 96-111 tumor necrosis factor Mus musculus 37-46 28628850-1 2017 BACKGROUND: Exposure of mice to D-galactosamine (GalN) and lipopolysaccharide (LPS) induces acute liver failure through elevation of TNF-alpha, which causes liver damage resembling that in humans. Galactosamine 49-53 tumor necrosis factor Mus musculus 133-142 28470665-5 2017 VLX103 decreased GalN/LPS induction of tumor necrosis factor (TNF) but had no effect on other proinflammatory cytokines. Galactosamine 17-21 tumor necrosis factor Mus musculus 39-60 28470665-5 2017 VLX103 decreased GalN/LPS induction of tumor necrosis factor (TNF) but had no effect on other proinflammatory cytokines. Galactosamine 17-21 tumor necrosis factor Mus musculus 62-65 26991125-4 2016 We report that lipopolysaccharide/galactosamine-induced liver injury depends on hepatocyte-intrinsic TNF receptor 1 (p55, TNFR1). Galactosamine 34-47 tumor necrosis factor Mus musculus 101-104 26141869-1 2015 BACKGROUND: Lipopolysaccharide/d-galactosamine (LPS/GalN)-induced hepatic injury is an experimental model of fulminant hepatic failure in which tumor necrosis factor alpha (TNF-alpha) plays a pivotal role. Galactosamine 31-46 tumor necrosis factor Mus musculus 173-182 25382719-4 2014 GalN/LPS increased serum tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) levels, while 1 attenuated TNF-alpha levels and further increased IL-6 levels. Galactosamine 0-4 tumor necrosis factor Mus musculus 25-52 26265045-3 2015 In the present study, the potential modulatory effects of metformin on TNF-alpha-dependent apoptotic liver damage was investigated in mice with TNF-alpha/d-galactosamine (D-Gal)-induced liver injury. Galactosamine 154-169 tumor necrosis factor Mus musculus 71-80 25325613-4 2014 Treatment with GalN/LPS resulted in increased levels of serum alanine aminotransferase, tumor necrosis factor (TNF)-alpha, and interleukin (IL)-6, as well as increased mortality, all of which were attenuated by treatment with 1. Galactosamine 15-19 tumor necrosis factor Mus musculus 88-121 26459629-1 2015 Treatment of mice with lipopolysaccharide (LPS) and the liver-specific transcriptional inhibitor D-(+)-galactosamine (GalN) induces fatal hepatitis, which is mediated by tumor necrosis factor alpha (TNF-alpha) and characterized by massive hepatic apoptosis. Galactosamine 97-116 tumor necrosis factor Mus musculus 170-197 26459629-1 2015 Treatment of mice with lipopolysaccharide (LPS) and the liver-specific transcriptional inhibitor D-(+)-galactosamine (GalN) induces fatal hepatitis, which is mediated by tumor necrosis factor alpha (TNF-alpha) and characterized by massive hepatic apoptosis. Galactosamine 97-116 tumor necrosis factor Mus musculus 199-208 26459629-1 2015 Treatment of mice with lipopolysaccharide (LPS) and the liver-specific transcriptional inhibitor D-(+)-galactosamine (GalN) induces fatal hepatitis, which is mediated by tumor necrosis factor alpha (TNF-alpha) and characterized by massive hepatic apoptosis. Galactosamine 118-122 tumor necrosis factor Mus musculus 170-197 26459629-1 2015 Treatment of mice with lipopolysaccharide (LPS) and the liver-specific transcriptional inhibitor D-(+)-galactosamine (GalN) induces fatal hepatitis, which is mediated by tumor necrosis factor alpha (TNF-alpha) and characterized by massive hepatic apoptosis. Galactosamine 118-122 tumor necrosis factor Mus musculus 199-208 26459629-5 2015 Moreover, targeted expression of Ifit1 in the liver by recombinant adeno-associated virus serotype 8 protected mice from LPS/GalN-induced lethal hepatitis, which was associated with the inhibition of TNF-alpha-mediated activation of the c-Jun N-terminal kinase (JNK)-Bim cascade. Galactosamine 125-129 tumor necrosis factor Mus musculus 200-209 26459629-7 2015 Together, our data demonstrate that Ifit1 is a novel protective factor that inhibits LPS/GalN-induced (TNF-alpha-mediated) fatal hepatitis, suggesting that Ifit1 is a potential therapeutic target for treatment of inflammatory liver diseases. Galactosamine 89-93 tumor necrosis factor Mus musculus 103-112 25325613-8 2014 Following GalN/LPS treatment, nuclear translocation of nuclear factor-kappaB and the levels of TNF-alpha and IL-6 mRNA expression increased, which were attenuated by 1. Galactosamine 10-14 tumor necrosis factor Mus musculus 95-104 25382719-4 2014 GalN/LPS increased serum tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) levels, while 1 attenuated TNF-alpha levels and further increased IL-6 levels. Galactosamine 0-4 tumor necrosis factor Mus musculus 54-63 25382719-4 2014 GalN/LPS increased serum tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) levels, while 1 attenuated TNF-alpha levels and further increased IL-6 levels. Galactosamine 0-4 tumor necrosis factor Mus musculus 117-126 22094102-6 2012 Down-regulation of TNFalpha in peritoneal CD11b+ monocytes reduced liver damage in C57BL/6 mice and significantly delayed acute mortality in mice treated with low dose LPS plus d-galactosamine (D-GalN). Galactosamine 177-192 tumor necrosis factor Mus musculus 19-27 24877692-6 2014 After 6h of GalN/LPS injection, the serum levels of alanine aminotransferase, aspartate aminotransferase, tumor necrosis factor (TNF)-alpha, interleukin-6 and interferon-gamma were significantly elevated. Galactosamine 12-16 tumor necrosis factor Mus musculus 106-139 23994575-9 2013 Serum levels of tumor necrosis factor-alpha (TNF-alpha) and interleukin (IL)-1beta increased after GalN/LPS treatment; these increases were attenuated by hemin. Galactosamine 99-103 tumor necrosis factor Mus musculus 16-43 23994575-9 2013 Serum levels of tumor necrosis factor-alpha (TNF-alpha) and interleukin (IL)-1beta increased after GalN/LPS treatment; these increases were attenuated by hemin. Galactosamine 99-103 tumor necrosis factor Mus musculus 45-54 23994575-10 2013 Hepatic mRNA levels of TNF-alpha, IL-1beta, and NLRP3 increased after GalN/LPS treatment, and hemin attenuated increases in TNF-alpha and IL-1beta. Galactosamine 70-74 tumor necrosis factor Mus musculus 23-32 19464067-4 2009 Immune-mediated liver injury was induced by administration of lipopolysaccharide (LPS) or tumor necrosis factor-alpha (TNFalpha) to galactosamine (GalN)-sensitized mice and evaluated by serum transaminase activities and cytokine levels. Galactosamine 132-145 tumor necrosis factor Mus musculus 90-117 22465962-1 2012 TNF alpha plays a central role in the pathogenesis of inflammatory diseases such as rheumatoid arthritis and murine acute liver injury induced by injection of D-galactosamine and subsequent LPS. Galactosamine 159-174 tumor necrosis factor Mus musculus 0-9 21928088-11 2012 The expression of TNF-alpha and interleukin (IL)-1beta were increased in the GalN/LPS group. Galactosamine 77-81 tumor necrosis factor Mus musculus 18-27 21253441-9 2011 injection with lethal dose of lipopolysaccharide (LPS)/D-galactosamine markedly reduced the levels of serum TNF-alpha and increased survival rates of animals from septic shock-induced death. Galactosamine 55-70 tumor necrosis factor Mus musculus 108-117 21899269-5 2011 Treatment with GalN/LPS induced an increase in the serum level of tumor necrosis factor-alpha (TNF-alpha) and protein expression of TNF-alpha receptor-associated death domain, and these increases were prevented by 1. Galactosamine 15-19 tumor necrosis factor Mus musculus 66-93 21899269-5 2011 Treatment with GalN/LPS induced an increase in the serum level of tumor necrosis factor-alpha (TNF-alpha) and protein expression of TNF-alpha receptor-associated death domain, and these increases were prevented by 1. Galactosamine 15-19 tumor necrosis factor Mus musculus 95-104 21899269-5 2011 Treatment with GalN/LPS induced an increase in the serum level of tumor necrosis factor-alpha (TNF-alpha) and protein expression of TNF-alpha receptor-associated death domain, and these increases were prevented by 1. Galactosamine 15-19 tumor necrosis factor Mus musculus 132-141 21063746-7 2011 CONCLUSIONS: Our experimental data indicated that Go6976, a PKD inhibitor, could effectively prevent LPS/D: -GalN-induced acute liver injury by inhibition of MAPKs activation to reduce TNF-alpha production. Galactosamine 109-113 tumor necrosis factor Mus musculus 185-194 20023007-8 2011 Further, it reduced the circulating TNF-alpha level, hepatic injury and mortality in mice receiving an injection of D-galactosamine and LPS. Galactosamine 116-131 tumor necrosis factor Mus musculus 36-45 19818826-9 2010 GalN/LPS increased the circulating levels of tumor necrosis factor (TNF)-alpha, interleukin-6 (IL-6) and IL-10. Galactosamine 0-4 tumor necrosis factor Mus musculus 45-78 19818826-11 2010 GalN/LPS treatment also increased the levels of TNF-alpha, IL-6 and IL-10 mRNA expression in liver tissue. Galactosamine 0-4 tumor necrosis factor Mus musculus 48-57 19464067-4 2009 Immune-mediated liver injury was induced by administration of lipopolysaccharide (LPS) or tumor necrosis factor-alpha (TNFalpha) to galactosamine (GalN)-sensitized mice and evaluated by serum transaminase activities and cytokine levels. Galactosamine 132-145 tumor necrosis factor Mus musculus 119-127 19249395-4 2009 METHODS: TNF-induced hepatocyte apoptosis was investigated in wild-type, jnk1-/- and jnk2-/- mice in vitro and in the galactosamine/TNF (GalN/TNF) liver injury model. Galactosamine 118-131 tumor necrosis factor Mus musculus 9-12 19264954-3 2009 Although it is well known that hepatocellular apoptosis in D-galactosamine/lipopolysaccharide (D-Gal/LPS)-associated liver failure is mediated by TNF-alpha-dependent Fas/FasL cytotoxicity, there is no information on the role of perforin-mediated mechanisms in vivo. Galactosamine 59-74 tumor necrosis factor Mus musculus 146-155 19119023-2 2009 Injection with lipopolysaccharide (LPS) plus the transcriptional inhibitor D(+)-galactosamine (GalN) or mitogenic T cell activation causes fatal hepatocyte apoptosis in mice, which is mediated by TNFalpha, but the effector mechanisms remain unclear. Galactosamine 75-93 tumor necrosis factor Mus musculus 196-204 19119023-2 2009 Injection with lipopolysaccharide (LPS) plus the transcriptional inhibitor D(+)-galactosamine (GalN) or mitogenic T cell activation causes fatal hepatocyte apoptosis in mice, which is mediated by TNFalpha, but the effector mechanisms remain unclear. Galactosamine 95-99 tumor necrosis factor Mus musculus 196-204 19001362-3 2009 Inhibition of hepatocyte apoptosis by pre-treatment with TNFalpha (TNFalpha tolerance) was analyzed in the mouse model of galactosamine/TNFalpha-induced liver injury and in actinomycin D/TNFalpha-treated primary mouse hepatocytes. Galactosamine 122-135 tumor necrosis factor Mus musculus 57-65 19001362-3 2009 Inhibition of hepatocyte apoptosis by pre-treatment with TNFalpha (TNFalpha tolerance) was analyzed in the mouse model of galactosamine/TNFalpha-induced liver injury and in actinomycin D/TNFalpha-treated primary mouse hepatocytes. Galactosamine 122-135 tumor necrosis factor Mus musculus 67-75 19001362-3 2009 Inhibition of hepatocyte apoptosis by pre-treatment with TNFalpha (TNFalpha tolerance) was analyzed in the mouse model of galactosamine/TNFalpha-induced liver injury and in actinomycin D/TNFalpha-treated primary mouse hepatocytes. Galactosamine 122-135 tumor necrosis factor Mus musculus 67-75 19001362-3 2009 Inhibition of hepatocyte apoptosis by pre-treatment with TNFalpha (TNFalpha tolerance) was analyzed in the mouse model of galactosamine/TNFalpha-induced liver injury and in actinomycin D/TNFalpha-treated primary mouse hepatocytes. Galactosamine 122-135 tumor necrosis factor Mus musculus 67-75 19001362-8 2009 Accordingly, c-Flip(L/S) protein levels were elevated in livers of TNFalpha-tolerant mice, which correlated to a switch from JNK and ERK to p38 signaling after galactosamine/TNF re-challenge. Galactosamine 160-173 tumor necrosis factor Mus musculus 67-75 19001362-8 2009 Accordingly, c-Flip(L/S) protein levels were elevated in livers of TNFalpha-tolerant mice, which correlated to a switch from JNK and ERK to p38 signaling after galactosamine/TNF re-challenge. Galactosamine 160-173 tumor necrosis factor Mus musculus 67-70 18946736-5 2008 Livers of galactosamine/lipopolysaccharide (Gal/LPS)-exposed Fas wild-type mice highly expressed both Fas and FasL and revealed marked hepatocellular apoptosis that was almost completely blocked by soluble TNFalpha-receptor; this was also almost absent in Gal/LPS-exposed Fas lymphoproliferation mutant mice. Galactosamine 10-23 tumor necrosis factor Mus musculus 206-214 17982095-3 2007 In this study, these mechanisms were investigated in murine hepatocyte cultures as well as in a mouse model of TNF-dependent apoptotic liver damage (galactosamine/TNF model). Galactosamine 149-162 tumor necrosis factor Mus musculus 111-114 18331798-0 2008 Tumor necrosis factor alpha mediates the lethal hepatotoxic effects of poly(I:C) in D-galactosamine-sensitized mice. Galactosamine 84-99 tumor necrosis factor Mus musculus 0-27 18215436-8 2008 Conversely, PDTC accelerated death and aggravated liver apoptosis in the GalN/LPS model, although it reduced nitric oxide production, attenuated glutathione depletion, and inhibited the expression of TNF-alpha in liver. Galactosamine 73-77 tumor necrosis factor Mus musculus 200-209 18378686-1 2008 Tumor necrosis factor-alpha (TNF-alpha) produced by macrophages in response to CpG DNA induces severe liver injury and subsequent death of D-galactosamine (D-GalN)-sensitized mice. Galactosamine 139-154 tumor necrosis factor Mus musculus 0-27 18378686-1 2008 Tumor necrosis factor-alpha (TNF-alpha) produced by macrophages in response to CpG DNA induces severe liver injury and subsequent death of D-galactosamine (D-GalN)-sensitized mice. Galactosamine 139-154 tumor necrosis factor Mus musculus 29-38 18379074-5 2008 These results suggest that acanthoic acid protects against D-galactosamine/lipopolysaccharide-induced fulminant liver failure at least in part by a mechanism associated with the down-regulation of TNF-alpha secretion. Galactosamine 59-74 tumor necrosis factor Mus musculus 197-206 18270473-9 2008 The elevation of serum tumor necrosis factor-alpha and activation of caspase-3 were observed in the GalN/LPS group, which was attenuated by gomisin A. Galactosamine 100-104 tumor necrosis factor Mus musculus 23-50 17372587-2 2007 It was recently reported that nonobese diabetic (NOD) mice are less sensitive to TNF-alpha/D-galactosamine (GalN)-induced liver failure than C57BL/6J (B6) mice, whereas both NOD and B6 mice were sensitive to the lethal effect of Jo-2. Galactosamine 108-112 tumor necrosis factor Mus musculus 81-90 17959032-3 2007 In the GalN/LPS model, TNF-alpha is the major mediator leading to apoptotic liver injury. Galactosamine 7-11 tumor necrosis factor Mus musculus 23-32 17959032-4 2007 Reactive oxygen species (ROS) are involved in GalN-induced sensitization to TNF-alpha-evoked hepatocyte apoptosis. Galactosamine 46-50 tumor necrosis factor Mus musculus 76-85 17224791-7 2007 In parallel, the levels of hepatic adenosine triphosphate increased significantly and were associated with a marked reduction of TNF-alpha-induced apoptosis in the liver of D-galactosamine-sensitized mice. Galactosamine 173-188 tumor necrosis factor Mus musculus 129-138 17463158-4 2007 Mice were treated with murine TNF-alpha via intravenous injection at 20 mug/kg body wt 30 mins after d-galactosamine (d-Gal) sensitization (800 mg/kg body wt). Galactosamine 101-116 tumor necrosis factor Mus musculus 30-39 17463158-4 2007 Mice were treated with murine TNF-alpha via intravenous injection at 20 mug/kg body wt 30 mins after d-galactosamine (d-Gal) sensitization (800 mg/kg body wt). Galactosamine 118-123 tumor necrosis factor Mus musculus 30-39 16832353-4 2006 TNF-alpha was injected into D-galactosamine (GalN)-sensitized mice that were pretreated with or without HS. Galactosamine 28-43 tumor necrosis factor Mus musculus 0-9 16979778-5 2006 JNK1 and JNK2 function was, therefore, investigated in the TNF-dependent, galactosamine/lipopolysaccharide (GalN/LPS) model of liver injury. Galactosamine 74-87 tumor necrosis factor Mus musculus 59-62 16983719-2 2006 Mutant mice produce physiologically regulated levels of transmembrane TNF (tmTNF), which suffice to support thymocyte proliferation but cannot substitute for the hepatotoxic activities of wild-type TNF following LPS/D-galactosamine challenge in vivo and are not sufficient to support secondary lymphoid organ structure and function. Galactosamine 216-231 tumor necrosis factor Mus musculus 70-73 16832353-4 2006 TNF-alpha was injected into D-galactosamine (GalN)-sensitized mice that were pretreated with or without HS. Galactosamine 45-49 tumor necrosis factor Mus musculus 0-9 16733851-4 2006 RESULTS: In knockout mice, GalN/LPS injection significantly lowered the survival rate, significantly raised the plasma levels of alanine transaminase and tumor necrosis factor-alpha (TNF-alpha) and significantly reduced IL-10 levels compared with wild type mice. Galactosamine 27-31 tumor necrosis factor Mus musculus 183-192 16399628-6 2006 All of TNF-alpha-deficient mice challenged with LPS+GalN survived. Galactosamine 52-56 tumor necrosis factor Mus musculus 7-16 16571730-3 2006 JNK1 and JNK2 function was, therefore, investigated in the TNF-dependent, galactosamine/lipopolysaccharide (GalN/LPS) model of liver injury. Galactosamine 74-87 tumor necrosis factor Mus musculus 59-62 16403638-3 2006 Inhibitory doses (ID50) of compounds 5 and 9 on TNFalpha production induced by coinjection of galactosamine and LPS in C3H/HeN mice in vivo were measured and were 0.55 and <0.20 mg/kg, respectively. Galactosamine 94-107 tumor necrosis factor Mus musculus 48-56 16051691-4 2005 Histamine attenuated the GalN/LPS-induced increases in the levels of TNF-alpha, but augmented those of IL-10 both in the liver and serum. Galactosamine 25-29 tumor necrosis factor Mus musculus 69-78 15968724-2 2005 METHODS: Liver damage was induced by lipopolysaccharide (LPS)/TNF-alpha in D-galactosamine (GalN) sensitized BALB/c mice. Galactosamine 75-90 tumor necrosis factor Mus musculus 62-71 16034092-11 2005 BALB/c mice were significantly less susceptible to alpha-GalCer-induced liver injury than C57BL/6 mice, in particular upon pretreatment with d-galactosamine, a hepatocyte-specific sensitizer to TNF-alpha-mediated injury. Galactosamine 141-156 tumor necrosis factor Mus musculus 194-203 15968724-2 2005 METHODS: Liver damage was induced by lipopolysaccharide (LPS)/TNF-alpha in D-galactosamine (GalN) sensitized BALB/c mice. Galactosamine 92-96 tumor necrosis factor Mus musculus 62-71 15942719-1 2005 BACKGROUND: D-Galactosamine (GalN)/lipopolysaccharide (LPS)-induced liver injury is an experimental model of fulminant hepatic failure in which tumor necrosis factor-alpha (TNF-alpha) plays a pivotal role. Galactosamine 29-33 tumor necrosis factor Mus musculus 144-171 15942719-1 2005 BACKGROUND: D-Galactosamine (GalN)/lipopolysaccharide (LPS)-induced liver injury is an experimental model of fulminant hepatic failure in which tumor necrosis factor-alpha (TNF-alpha) plays a pivotal role. Galactosamine 29-33 tumor necrosis factor Mus musculus 173-182 15942719-1 2005 BACKGROUND: D-Galactosamine (GalN)/lipopolysaccharide (LPS)-induced liver injury is an experimental model of fulminant hepatic failure in which tumor necrosis factor-alpha (TNF-alpha) plays a pivotal role. Galactosamine 12-27 tumor necrosis factor Mus musculus 144-171 15942719-1 2005 BACKGROUND: D-Galactosamine (GalN)/lipopolysaccharide (LPS)-induced liver injury is an experimental model of fulminant hepatic failure in which tumor necrosis factor-alpha (TNF-alpha) plays a pivotal role. Galactosamine 12-27 tumor necrosis factor Mus musculus 173-182 15850520-2 2005 METHODS: Liver damage was induced by lipopolysaccharide (LPS)/TNFalpha in D-galactosamine (GalN) sensitized BALB/c mice. Galactosamine 74-89 tumor necrosis factor Mus musculus 62-70 15356173-4 2004 After injection of LPS/2-amino-2-deoxy-D-galactose (D-gal), CD137-/- mice had reduced serum cytokine levels and substantially impaired liver IFN-gamma and TNF-alpha mRNA levels. Galactosamine 23-50 tumor necrosis factor Mus musculus 155-164 15461564-5 2004 In mice, D-galactosamine and endotoxin cause apoptotic liver damage, which is mediated by TNF. Galactosamine 9-24 tumor necrosis factor Mus musculus 90-93 15003809-2 2004 An endotoxicosis model that utilizes LPS and d-galactosamine to induce mortality by TNFalpha/TNFR1-dependent hepatocyte apoptosis was used to assess TNFalpha production, apoptotic signaling, and effects on the production of IL-6 and IL-10. Galactosamine 45-60 tumor necrosis factor Mus musculus 84-92 15239101-7 2004 In addition, pretreatment with adiponectin attenuated the GalN/LPS-induced increases in serum and hepatic tumor necrosis factor alpha (TNF-alpha) levels and increased peroxisome proliferator-activated receptor (PPAR) alpha messenger RNA expression in the liver. Galactosamine 58-62 tumor necrosis factor Mus musculus 106-133 15239101-7 2004 In addition, pretreatment with adiponectin attenuated the GalN/LPS-induced increases in serum and hepatic tumor necrosis factor alpha (TNF-alpha) levels and increased peroxisome proliferator-activated receptor (PPAR) alpha messenger RNA expression in the liver. Galactosamine 58-62 tumor necrosis factor Mus musculus 135-144 15043992-1 2004 The effects of secoisolariciresinol (1) and isotaxiresinol (2), two major lignans isolated from the wood of Taxus yunnanensis, on tumor necrosis factor-alpha (TNF-alpha)-dependent hepatic apoptosis induced by D-galactosamine (d-GalN)/lipopolysaccharide (LPS) were investigated in mice. Galactosamine 209-224 tumor necrosis factor Mus musculus 159-168 14617692-10 2004 Similar results were obtained when apoptotic liver damage was induced by administration of tumor necrosis factor-alpha to d-galactosamine-sensitized mice. Galactosamine 122-137 tumor necrosis factor Mus musculus 91-118 14978949-10 2004 We report that Sho-saiko-to decreases the rh TNF-induced lethality in galactosamine-hypersensitized mice and protects mice against oxygen toxicity and Ca2+ overload in the cytoplasm or mitochondria during endotoxemia. Galactosamine 70-83 tumor necrosis factor Mus musculus 45-48 12365717-10 2002 By treating the cells, galactosamine and cycloheximide also lowered the apoptosis-inducing activity and decreased TNF-alpha and IL-2 productions. Galactosamine 23-36 tumor necrosis factor Mus musculus 114-123 15198850-1 2004 D-Galactosamine (D-galN) is well established as sensitizing mice and other animals to the lethal effects of TNF, specifically, and by several orders of magnitude. Galactosamine 0-15 tumor necrosis factor Mus musculus 108-111 12649350-10 2003 NK-1R blockade clearly inhibited GalN/LPS-induced production of TNFalpha and IFNgamma, whereas synthesis of the hepatoprotective cytokines IL-6 and IL-10 was increased. Galactosamine 33-37 tumor necrosis factor Mus musculus 64-72 12486082-0 2002 NFkappaB and caspase-3 activity in apoptotic hepatocytes of galactosamine-sensitized mice treated with TNFalpha. Galactosamine 60-73 tumor necrosis factor Mus musculus 103-111 12486082-1 2002 Tumor necrosis factor-alpha (TNFalpha) induces apoptosis in hepatocytes only under transcriptional arrest induced by galactosamine (GalN). Galactosamine 117-130 tumor necrosis factor Mus musculus 0-27 12486082-1 2002 Tumor necrosis factor-alpha (TNFalpha) induces apoptosis in hepatocytes only under transcriptional arrest induced by galactosamine (GalN). Galactosamine 117-130 tumor necrosis factor Mus musculus 29-37 12486082-1 2002 Tumor necrosis factor-alpha (TNFalpha) induces apoptosis in hepatocytes only under transcriptional arrest induced by galactosamine (GalN). Galactosamine 132-136 tumor necrosis factor Mus musculus 0-27 12486082-1 2002 Tumor necrosis factor-alpha (TNFalpha) induces apoptosis in hepatocytes only under transcriptional arrest induced by galactosamine (GalN). Galactosamine 132-136 tumor necrosis factor Mus musculus 29-37 12531875-5 2003 Furthermore, although in vivo administration of TNF-alpha or LPS to galactosamine-pretreated ASMase(+/+) mice caused liver damage, ASMase(-/-) mice exhibited minimal hepatocellular injury. Galactosamine 68-81 tumor necrosis factor Mus musculus 48-57 12056510-0 2002 TNF tolerance and cytotoxicity in the liver: the role of interleukin-1beta, inducible nitric oxide-synthase and heme oxygenase-1 in D-galactosamine-sensitized mice. Galactosamine 132-147 tumor necrosis factor Mus musculus 0-3 12098599-6 2002 A single oral administration of pirfenidone prior to lipopolysaccharide/D-galactosamine challenge inhibited the production of circulating tumor necrosis factor-alpha (TNF-alpha), interleukin-12 and interferon-gamma, markedly enhanced that of interleukin-10, and offered protection from subsequent lethal symptoms in a dose-dependent manner. Galactosamine 72-87 tumor necrosis factor Mus musculus 138-165 12056510-3 2002 Liver damage was induced by administration of TNF to mice sensitized with D-galactosamine (GalN). Galactosamine 74-89 tumor necrosis factor Mus musculus 46-49 12056510-3 2002 Liver damage was induced by administration of TNF to mice sensitized with D-galactosamine (GalN). Galactosamine 91-95 tumor necrosis factor Mus musculus 46-49 11983446-7 2002 RESULTS: Pretreatment of mice with 4-nitrobenzylidene malononitrile reduced tumor necrosis factor-alpha/D-galactosamine-induced hepatotoxicity. Galactosamine 106-119 tumor necrosis factor Mus musculus 76-103 11369777-3 2001 After treating mice with lipopolysaccharide or TNFalpha in the presence of d-galactosamine, Bid was cleaved and translocated to mitochondria in hepatocytes. Galactosamine 75-90 tumor necrosis factor Mus musculus 47-55 12537698-0 2002 Does high mobility group 1 protein function as a late mediator for LPS- or TNF-induced shock in galactosamine-sensitized mice? Galactosamine 96-109 tumor necrosis factor Mus musculus 75-78 12537698-1 2002 The role of high mobility group-1 protein (HMG-1) in LPS- and TNF-alpha-induced lethal shock in galactosamine (GalN)-sensitized mice was investigated. Galactosamine 96-109 tumor necrosis factor Mus musculus 62-71 12537698-4 2002 When GalN-sensitized mice were injected with TNF-alpha, the presence of HMG-1 was seen at 5.5 h in plasma of BALB/c mice and at 6 h in BALB/lps(d) mice, although almost all GalN-sensitized BALB/c mice died by 6 h after challenge. Galactosamine 5-9 tumor necrosis factor Mus musculus 45-54 12537698-4 2002 When GalN-sensitized mice were injected with TNF-alpha, the presence of HMG-1 was seen at 5.5 h in plasma of BALB/c mice and at 6 h in BALB/lps(d) mice, although almost all GalN-sensitized BALB/c mice died by 6 h after challenge. Galactosamine 173-177 tumor necrosis factor Mus musculus 45-54 11589767-0 2001 Caspase activation during hepatocyte apoptosis induced by tumor necrosis factor-alpha in galactosamine-sensitized mice. Galactosamine 89-102 tumor necrosis factor Mus musculus 58-85 11589767-1 2001 BACKGROUND/AIMS: To clarify the mechanism of hepatocyte apoptosis induced by tumor necrosis factor-alpha (TNF-alpha), caspase cascade and ceramide formation were investigated in the liver of D-galactosamine (GalN)-sensitized mice treated with TNF-alpha. Galactosamine 191-206 tumor necrosis factor Mus musculus 77-104 11391533-1 2001 D-Galactosamine (GalN)/lipopolysaccharide (LPS)-induced liver injury is an experimental model of fulminant hepatic failure in which tumor necrosis factor alpha (TNF-alpha) plays a pivotal role. Galactosamine 0-15 tumor necrosis factor Mus musculus 132-159 11500080-2 2001 Galactosamine (GalN) sensitises experimental animals for TNF and the combination TNF/GalN leads to a lethal inflammatory hepatitis. Galactosamine 15-19 tumor necrosis factor Mus musculus 57-60 11500080-2 2001 Galactosamine (GalN) sensitises experimental animals for TNF and the combination TNF/GalN leads to a lethal inflammatory hepatitis. Galactosamine 0-13 tumor necrosis factor Mus musculus 57-60 11391533-1 2001 D-Galactosamine (GalN)/lipopolysaccharide (LPS)-induced liver injury is an experimental model of fulminant hepatic failure in which tumor necrosis factor alpha (TNF-alpha) plays a pivotal role. Galactosamine 0-15 tumor necrosis factor Mus musculus 161-170 11391533-1 2001 D-Galactosamine (GalN)/lipopolysaccharide (LPS)-induced liver injury is an experimental model of fulminant hepatic failure in which tumor necrosis factor alpha (TNF-alpha) plays a pivotal role. Galactosamine 17-21 tumor necrosis factor Mus musculus 132-159 11391533-1 2001 D-Galactosamine (GalN)/lipopolysaccharide (LPS)-induced liver injury is an experimental model of fulminant hepatic failure in which tumor necrosis factor alpha (TNF-alpha) plays a pivotal role. Galactosamine 17-21 tumor necrosis factor Mus musculus 161-170 11319761-0 2001 Possible involvement of reactive oxygen species in D-galactosamine-induced sensitization against tumor necrosis factor-alpha-induced hepatocyte apoptosis. Galactosamine 51-66 tumor necrosis factor Mus musculus 97-124 11319761-1 2001 Intravenous administration of tumor necrosis factor-alpha (TNF-alpha) (0.5 microg/mouse) caused hepatocyte apoptosis in BALB/c mice when they were sensitized with D-galactosamine (GalN, 20 mg/mouse). Galactosamine 180-184 tumor necrosis factor Mus musculus 59-68 11093734-2 2000 Pretreatment with TNF-alpha or interleukin-1beta (IL-1beta), which activated NF-kappaB in the liver, dramatically prevented TNF-alpha-induced liver-cell apoptosis in D-galactosamine (GalN)-sensitized mice, but not anti-Fas antibody-induced hepatotoxicity. Galactosamine 166-181 tumor necrosis factor Mus musculus 18-27 11319761-11 2001 These results suggest that ROS produced by GalN may play a pivotal role in hepatocyte sensitization toward TNF-alpha-induced apoptosis. Galactosamine 43-47 tumor necrosis factor Mus musculus 107-116 11181643-6 2001 iNOS-/- mice were protected from liver damage after Con A treatment, as well as in another TNF-alpha-mediated model that is inducible by LPS in D-galactosamine-sensitized (GalN-sensitized) mice. Galactosamine 144-159 tumor necrosis factor Mus musculus 91-100 11181643-6 2001 iNOS-/- mice were protected from liver damage after Con A treatment, as well as in another TNF-alpha-mediated model that is inducible by LPS in D-galactosamine-sensitized (GalN-sensitized) mice. Galactosamine 172-176 tumor necrosis factor Mus musculus 91-100 11242124-7 2001 D-galactosamine adenovirus vector can partially reduced hepatocyte apoptosis induced by TNF- alpha and D-galactosamine. Galactosamine 2-15 tumor necrosis factor Mus musculus 88-98 11242124-7 2001 D-galactosamine adenovirus vector can partially reduced hepatocyte apoptosis induced by TNF- alpha and D-galactosamine. Galactosamine 0-15 tumor necrosis factor Mus musculus 88-98 11242125-2 2001 METHODS: Fulminant hepatic failure (FHF) was induced by injection of GalN into sensitized BALB/c mice by TNF-alpha. Galactosamine 69-73 tumor necrosis factor Mus musculus 105-114 11093734-2 2000 Pretreatment with TNF-alpha or interleukin-1beta (IL-1beta), which activated NF-kappaB in the liver, dramatically prevented TNF-alpha-induced liver-cell apoptosis in D-galactosamine (GalN)-sensitized mice, but not anti-Fas antibody-induced hepatotoxicity. Galactosamine 183-187 tumor necrosis factor Mus musculus 124-133 11319761-1 2001 Intravenous administration of tumor necrosis factor-alpha (TNF-alpha) (0.5 microg/mouse) caused hepatocyte apoptosis in BALB/c mice when they were sensitized with D-galactosamine (GalN, 20 mg/mouse). Galactosamine 163-178 tumor necrosis factor Mus musculus 30-57 11319761-1 2001 Intravenous administration of tumor necrosis factor-alpha (TNF-alpha) (0.5 microg/mouse) caused hepatocyte apoptosis in BALB/c mice when they were sensitized with D-galactosamine (GalN, 20 mg/mouse). Galactosamine 163-178 tumor necrosis factor Mus musculus 59-68 11319761-1 2001 Intravenous administration of tumor necrosis factor-alpha (TNF-alpha) (0.5 microg/mouse) caused hepatocyte apoptosis in BALB/c mice when they were sensitized with D-galactosamine (GalN, 20 mg/mouse). Galactosamine 180-184 tumor necrosis factor Mus musculus 30-57 11525242-1 2001 Tumor necrosis factor-alpha (TNFalpha) could cause apoptosis in hepatic tissue of D-galactosamine sensitized mice, as evidenced by the increase in the extent of DNA fragmentation. Galactosamine 82-97 tumor necrosis factor Mus musculus 0-27 11525242-1 2001 Tumor necrosis factor-alpha (TNFalpha) could cause apoptosis in hepatic tissue of D-galactosamine sensitized mice, as evidenced by the increase in the extent of DNA fragmentation. Galactosamine 82-97 tumor necrosis factor Mus musculus 29-37 11753206-1 2001 Lipopolysaccharide and D-galactosamine induced lethality and apoptotic liver injury is dependent upon endogenously produced TNF-alpha. Galactosamine 23-38 tumor necrosis factor Mus musculus 124-133 11753206-3 2001 In a series of recent studies, we have demonstrated that mortality and hepatic injury following lipopolysaccharide administration in D-galactosamine-sensitized mice is dependent upon secreted 17 kDa TNF-alpha acting primarily through the p55 TNF receptor. Galactosamine 133-148 tumor necrosis factor Mus musculus 199-208 11753206-4 2001 Transgenic mice expressing null forms of TNF-alpha, the p55 receptor, or expressing only a cell-associated form of TNF-alpha exhibited no mortality and only modest liver injury when challenged with 8 mg of D-galactosamine and 100 ng of lipopolysaccharide. Galactosamine 206-221 tumor necrosis factor Mus musculus 115-124 11753206-8 2001 The studies confirm an essential role for TNF-alpha and p55 TNF receptor signaling in the hepatocyte apoptosis and lethality associated with lipopolysaccharide and D-galactosamine administration. Galactosamine 164-179 tumor necrosis factor Mus musculus 42-51 11093734-2 2000 Pretreatment with TNF-alpha or interleukin-1beta (IL-1beta), which activated NF-kappaB in the liver, dramatically prevented TNF-alpha-induced liver-cell apoptosis in D-galactosamine (GalN)-sensitized mice, but not anti-Fas antibody-induced hepatotoxicity. Galactosamine 166-181 tumor necrosis factor Mus musculus 124-133 11093734-2 2000 Pretreatment with TNF-alpha or interleukin-1beta (IL-1beta), which activated NF-kappaB in the liver, dramatically prevented TNF-alpha-induced liver-cell apoptosis in D-galactosamine (GalN)-sensitized mice, but not anti-Fas antibody-induced hepatotoxicity. Galactosamine 183-187 tumor necrosis factor Mus musculus 18-27 11086099-9 2000 The resistance to LPS- and TNF-alpha-mediated lethality and hepatic injury in D-galactosamine-sensitized NOD mice is apparently due to a post-TNFR binding defect, and independent of signaling pathways shared with Fas. Galactosamine 78-93 tumor necrosis factor Mus musculus 27-36 11125302-7 2000 In D-(+)-galactosamine (GalN)-sensitized mice, TNF induces lethal inflammatory hepatitis. Galactosamine 3-22 tumor necrosis factor Mus musculus 47-50 11125302-7 2000 In D-(+)-galactosamine (GalN)-sensitized mice, TNF induces lethal inflammatory hepatitis. Galactosamine 24-28 tumor necrosis factor Mus musculus 47-50 10948120-1 2000 The proinflammatory cytokine tumor necrosis factor alpha (TNF-alpha) induces lethal hepatitis when injected into D-(+)-galactosamine-sensitized mice on the one hand or systemic inflammatory response syndrome (SIRS) in normal mice on the other hand. Galactosamine 113-132 tumor necrosis factor Mus musculus 29-56 11090702-0 2000 Modification of tumor necrosis factor-induced acute toxicity D-galactosamine challenge by polymyxin B, an anti-endotoxin. Galactosamine 61-76 tumor necrosis factor Mus musculus 16-37 11090702-12 2000 and GalN, and these animals showed 100% mortality at 8 h. These findings suggested that the extent of TNF-induced toxicity caused by GalN administration may be a result of synergism between TNF and gut-derived endotoxin. Galactosamine 133-137 tumor necrosis factor Mus musculus 102-105 11090702-12 2000 and GalN, and these animals showed 100% mortality at 8 h. These findings suggested that the extent of TNF-induced toxicity caused by GalN administration may be a result of synergism between TNF and gut-derived endotoxin. Galactosamine 133-137 tumor necrosis factor Mus musculus 190-193 10948120-1 2000 The proinflammatory cytokine tumor necrosis factor alpha (TNF-alpha) induces lethal hepatitis when injected into D-(+)-galactosamine-sensitized mice on the one hand or systemic inflammatory response syndrome (SIRS) in normal mice on the other hand. Galactosamine 113-132 tumor necrosis factor Mus musculus 58-67 10801287-0 2000 Lipopolysaccharide and D-galactosamine-induced hepatic injury is mediated by TNF-alpha and not by Fas ligand. Galactosamine 23-38 tumor necrosis factor Mus musculus 77-86 10988358-4 2000 On the other hand, DFX prevents mortality induced either by LPS or murine recombinant TNF-alpha in D(+)-galactosamine (GalN)-sensitized mice. Galactosamine 99-117 tumor necrosis factor Mus musculus 86-95 10988358-4 2000 On the other hand, DFX prevents mortality induced either by LPS or murine recombinant TNF-alpha in D(+)-galactosamine (GalN)-sensitized mice. Galactosamine 119-123 tumor necrosis factor Mus musculus 86-95 10988358-5 2000 These protective actions of DFX correlate with an attenuated tissue damage observed in lungs, livers and kidneys of LPS-treated animals and GalN-sensitized mice inoculated with TNF-alpha. Galactosamine 140-144 tumor necrosis factor Mus musculus 177-186 10801287-7 2000 We conclude that the shock and apoptotic liver injury after D-galactosamine/lipopolysaccharide treatment are due primarily to TNF-alpha release, whereas increased FasL expression appears to contribute little to the mortality and hepatic injury. Galactosamine 60-75 tumor necrosis factor Mus musculus 126-135 10801288-0 2000 LPS-induced liver injury in D-galactosamine-sensitized mice requires secreted TNF-alpha and the TNF-p55 receptor. Galactosamine 28-43 tumor necrosis factor Mus musculus 78-87 10801287-3 2000 Here, we report that D-galactosamine and lipopolysaccharide-induced liver injury in C57BL/6 mice is associated with increased hepatic expression of both TNF-alpha and FasL mRNA. Galactosamine 21-36 tumor necrosis factor Mus musculus 153-162 10801288-1 2000 Lipopolysaccharide and D-galactosamine induced lethality and apoptotic liver injury is dependent on endogenously produced tumor necrosis factor (TNF)-alpha. Galactosamine 23-38 tumor necrosis factor Mus musculus 122-155 10801288-7 2000 We conclude that survival and apoptotic liver injury in response to lipopolysaccharide and D-galactosamine are dependent exclusively on secreted TNF-alpha signaling through the p55 receptor. Galactosamine 91-106 tumor necrosis factor Mus musculus 145-154 10675538-3 2000 In order to increase the therapeutic value of TNF, we have studied the protective activity of several molecules and found that four chemically totally different substances confer significant protection in the model of TNF-induced lethal hepatitis in mice sensitized with D-(+)-galactosamine (GalN), but not in mice sensitized with actinomycin-D (ActD) or against anti-Fas-induced lethal hepatitis. Galactosamine 271-290 tumor necrosis factor Mus musculus 46-49 10785422-3 2000 Among the new triterpene glucosides, three compounds (1, 2, 5) showed significant hepatoprotective effects against D-galactosamine (D-GalN)/tumor necrosis factor-alpha (TNF-alpha)-induced cell death in primary cultured mouse hepatocytes. Galactosamine 115-130 tumor necrosis factor Mus musculus 169-178 10675538-3 2000 In order to increase the therapeutic value of TNF, we have studied the protective activity of several molecules and found that four chemically totally different substances confer significant protection in the model of TNF-induced lethal hepatitis in mice sensitized with D-(+)-galactosamine (GalN), but not in mice sensitized with actinomycin-D (ActD) or against anti-Fas-induced lethal hepatitis. Galactosamine 271-290 tumor necrosis factor Mus musculus 218-221 10675538-3 2000 In order to increase the therapeutic value of TNF, we have studied the protective activity of several molecules and found that four chemically totally different substances confer significant protection in the model of TNF-induced lethal hepatitis in mice sensitized with D-(+)-galactosamine (GalN), but not in mice sensitized with actinomycin-D (ActD) or against anti-Fas-induced lethal hepatitis. Galactosamine 292-296 tumor necrosis factor Mus musculus 218-221 10706424-0 2000 Role of endogenous endotoxin on tumor necrosis factor-hypersensitivity caused by D-galactosamine challenge. Galactosamine 81-96 tumor necrosis factor Mus musculus 32-53 10498828-19 1999 Possibly, production of this hepatocyte-derived TNF-down-regulator (TNF-DRh) may be: (i) inhibited by GalN, causing over-production of TNF by macrophages and (ii) stimulated by LPS-pretreatment (and restored by uridine), causing reduced TNF production. Galactosamine 102-106 tumor necrosis factor Mus musculus 68-71 10580578-1 1999 BACKGROUND/AIMS: Proinflammatory cytokines including tumor necrosis factor alpha (TNF-alpha) and interferon gamma (IFN-gamma) play a critical role in the pathogenesis of liver injury induced by lipopolysaccharide (LPS) or staphylococcal enterotoxin B (SEB) in D-galactosamine (GalN)-sensitized mice. Galactosamine 260-275 tumor necrosis factor Mus musculus 53-80 10580578-1 1999 BACKGROUND/AIMS: Proinflammatory cytokines including tumor necrosis factor alpha (TNF-alpha) and interferon gamma (IFN-gamma) play a critical role in the pathogenesis of liver injury induced by lipopolysaccharide (LPS) or staphylococcal enterotoxin B (SEB) in D-galactosamine (GalN)-sensitized mice. Galactosamine 260-275 tumor necrosis factor Mus musculus 82-91 10580578-1 1999 BACKGROUND/AIMS: Proinflammatory cytokines including tumor necrosis factor alpha (TNF-alpha) and interferon gamma (IFN-gamma) play a critical role in the pathogenesis of liver injury induced by lipopolysaccharide (LPS) or staphylococcal enterotoxin B (SEB) in D-galactosamine (GalN)-sensitized mice. Galactosamine 277-281 tumor necrosis factor Mus musculus 53-80 10580578-1 1999 BACKGROUND/AIMS: Proinflammatory cytokines including tumor necrosis factor alpha (TNF-alpha) and interferon gamma (IFN-gamma) play a critical role in the pathogenesis of liver injury induced by lipopolysaccharide (LPS) or staphylococcal enterotoxin B (SEB) in D-galactosamine (GalN)-sensitized mice. Galactosamine 277-281 tumor necrosis factor Mus musculus 82-91 10549870-0 1999 D-galactosamine-induced mouse hepatic apoptosis: possible involvement with tumor necrosis factor, but not with caspase-3 activity. Galactosamine 0-15 tumor necrosis factor Mus musculus 75-96 10549870-1 1999 We investigated whether tumor necrosis factor (TNF) and caspase-3 activity are involved in the induction of hepatocellular apoptosis in D-galactosamine (D-GalN)-induced hepatotoxicity in mice. Galactosamine 136-151 tumor necrosis factor Mus musculus 24-45 10549870-1 1999 We investigated whether tumor necrosis factor (TNF) and caspase-3 activity are involved in the induction of hepatocellular apoptosis in D-galactosamine (D-GalN)-induced hepatotoxicity in mice. Galactosamine 136-151 tumor necrosis factor Mus musculus 47-50 10604572-2 1999 The aims of this study were to assess the differences between liver cell deaths induced by TNF-alpha and anti-Fas antibody, and to investigate the mechanism by which GalN sensitizes the hepatocyte to injury by TNF-alpha. Galactosamine 166-170 tumor necrosis factor Mus musculus 210-219 10604572-3 1999 METHODS: TNF-alpha or anti-Fas antibody was injected into BALB/c mice sensitized or unsensitized by D-galactosamine (GalN). Galactosamine 100-115 tumor necrosis factor Mus musculus 9-18 10604572-3 1999 METHODS: TNF-alpha or anti-Fas antibody was injected into BALB/c mice sensitized or unsensitized by D-galactosamine (GalN). Galactosamine 117-121 tumor necrosis factor Mus musculus 9-18 10604572-7 1999 RESULTS: In GalN-sensitized mice, hepatocyte apoptosis and liver failure were observed after TNF-alpha injection, but neither occurred in unsensitized mice. Galactosamine 12-16 tumor necrosis factor Mus musculus 93-102 10604572-9 1999 TNFR1 mRNA expression in the liver was upregulated within 3 h after GalN administration, and anti-TNFR1 antibody protected GalN-sensitized mice from hepatotoxic effects of TNF-alpha. Galactosamine 123-127 tumor necrosis factor Mus musculus 172-181 10553044-1 1999 Lethal hepatitis can be induced by an agonistic anti-Fas Ab in normal mice or by TNF in mice sensitized to d -(+)-galactosamine or actinomycin D. Galactosamine 107-127 tumor necrosis factor Mus musculus 81-84 10534346-2 1999 Injection of TNF or T-cell-activating agents (i.e., agonistic anti-CD3 antibody or staphylococcal enterotoxin B [SEB]) into galactosamine (GalN)-sensitized mice caused TNF/TNF-R1-dependent liver injury. Galactosamine 124-137 tumor necrosis factor Mus musculus 13-16 10534346-2 1999 Injection of TNF or T-cell-activating agents (i.e., agonistic anti-CD3 antibody or staphylococcal enterotoxin B [SEB]) into galactosamine (GalN)-sensitized mice caused TNF/TNF-R1-dependent liver injury. Galactosamine 139-143 tumor necrosis factor Mus musculus 13-16 10534346-2 1999 Injection of TNF or T-cell-activating agents (i.e., agonistic anti-CD3 antibody or staphylococcal enterotoxin B [SEB]) into galactosamine (GalN)-sensitized mice caused TNF/TNF-R1-dependent liver injury. Galactosamine 139-143 tumor necrosis factor Mus musculus 168-171 10534346-5 1999 Consistently, the broad-spectrum caspase inhibitor, benzoyloxycarbonyl-val-ala-asp-fluoromethylketone (zVADfmk), prevented TNF-mediated hepatotoxicity in all GalN-dependent models, but failed to protect against Con A. Galactosamine 158-162 tumor necrosis factor Mus musculus 123-126 10353265-1 1999 We investigated the effect of tetrahydroswertianolin (THS), a hepatoprotective agent from Swertia japonica, on tumor necrosis factor-alpha (TNF-alpha)-dependent hepatic apoptosis induced by D-galactosamine (D-GalN) (700 mg/kg, i.p.) Galactosamine 190-205 tumor necrosis factor Mus musculus 140-149 10498828-0 1999 Enhancement by galactosamine of lipopolysaccharide(LPS)-induced tumour necrosis factor production and lethality: its suppression by LPS pretreatment. Galactosamine 15-28 tumor necrosis factor Mus musculus 64-86 10498828-8 1999 Intraperitoneal injection of GalN+LPS into mice greatly elevated serum TNF. Galactosamine 29-33 tumor necrosis factor Mus musculus 71-74 10498828-10 1999 Administration of a macrophage depletor, liposomes encapsulated with dichloromethylene bisphosphonate, reduced both the TNF production and mortality induced by GalN+LPS. Galactosamine 160-164 tumor necrosis factor Mus musculus 120-123 10498828-12 1999 Uridine, when injected 0.5 h after the injection of GalN+LPS, reduced the production of TNF. Galactosamine 52-56 tumor necrosis factor Mus musculus 88-91 10498828-15 1999 Serum from LPS-injected mice reduced the TNF production induced by GalN+LPS, but it was less effective at reducing the lethality. Galactosamine 67-71 tumor necrosis factor Mus musculus 41-44 10498828-19 1999 Possibly, production of this hepatocyte-derived TNF-down-regulator (TNF-DRh) may be: (i) inhibited by GalN, causing over-production of TNF by macrophages and (ii) stimulated by LPS-pretreatment (and restored by uridine), causing reduced TNF production. Galactosamine 102-106 tumor necrosis factor Mus musculus 48-51 10498828-19 1999 Possibly, production of this hepatocyte-derived TNF-down-regulator (TNF-DRh) may be: (i) inhibited by GalN, causing over-production of TNF by macrophages and (ii) stimulated by LPS-pretreatment (and restored by uridine), causing reduced TNF production. Galactosamine 102-106 tumor necrosis factor Mus musculus 68-71 10498828-19 1999 Possibly, production of this hepatocyte-derived TNF-down-regulator (TNF-DRh) may be: (i) inhibited by GalN, causing over-production of TNF by macrophages and (ii) stimulated by LPS-pretreatment (and restored by uridine), causing reduced TNF production. Galactosamine 102-106 tumor necrosis factor Mus musculus 68-71 10433810-1 1999 Injection of tumour necrosis factor (TNF) in animals causes severe liver cell toxicity, especially when D-(+)-galactosamine (GalN) is co-administered. Galactosamine 104-123 tumor necrosis factor Mus musculus 13-35 10433810-1 1999 Injection of tumour necrosis factor (TNF) in animals causes severe liver cell toxicity, especially when D-(+)-galactosamine (GalN) is co-administered. Galactosamine 104-123 tumor necrosis factor Mus musculus 37-40 10433810-1 1999 Injection of tumour necrosis factor (TNF) in animals causes severe liver cell toxicity, especially when D-(+)-galactosamine (GalN) is co-administered. Galactosamine 125-129 tumor necrosis factor Mus musculus 13-35 10433810-1 1999 Injection of tumour necrosis factor (TNF) in animals causes severe liver cell toxicity, especially when D-(+)-galactosamine (GalN) is co-administered. Galactosamine 125-129 tumor necrosis factor Mus musculus 37-40 10229108-5 1999 Our results also show that, in contrast to expectations, IL4-/- mice are more susceptible to SEB plus low-dose D-galactosamine-induced shock and that this response is TNF-alpha-dependent. Galactosamine 111-126 tumor necrosis factor Mus musculus 167-176 10337911-1 1999 To investigate the interaction between the peripheral nervous and the immune system in vivo, we used two mouse models of T cell and TNF-alpha dependent liver injury inducible by either concanavalin A or a combination of D-galactosamine and staphylococcal enterotoxin B. Galactosamine 220-235 tumor necrosis factor Mus musculus 132-141 10194182-8 1999 LPS toxicity in D-galactosamine-treated mice, leading to blocked gene transcription, results from tumor necrosis factor (TNF)-alpha-induced caspase-3-dependent liver injury, not from the systemic inflammatory response. Galactosamine 16-31 tumor necrosis factor Mus musculus 98-131 10341451-2 1998 Although its exact biological function remains controversial, it was shown to protect galactosamine-sensitized or normal mice against hepatitis and lethal shock induced by tumor necrosis factor (TNF). Galactosamine 86-99 tumor necrosis factor Mus musculus 172-193 10668460-0 1999 Ultrastructural alterations of mitochondria in pre-apoptotic and apoptotic hepatocytes of TNF alpha-treated galactosamine-sensitized mice. Galactosamine 108-121 tumor necrosis factor Mus musculus 90-99 10341451-2 1998 Although its exact biological function remains controversial, it was shown to protect galactosamine-sensitized or normal mice against hepatitis and lethal shock induced by tumor necrosis factor (TNF). Galactosamine 86-99 tumor necrosis factor Mus musculus 195-198 9742073-0 1998 Pre-apoptotic alterations in hepatocytes of TNFalpha-treated galactosamine-sensitized mice. Galactosamine 61-74 tumor necrosis factor Mus musculus 44-52 9742073-1 1998 Tumor necrosis factor (TNF) induces apoptotic death of hepatocytes in the galactosamine (GalN)-sensitized mouse liver after 5 hr. Galactosamine 74-87 tumor necrosis factor Mus musculus 0-21 9742073-1 1998 Tumor necrosis factor (TNF) induces apoptotic death of hepatocytes in the galactosamine (GalN)-sensitized mouse liver after 5 hr. Galactosamine 74-87 tumor necrosis factor Mus musculus 23-26 9742073-1 1998 Tumor necrosis factor (TNF) induces apoptotic death of hepatocytes in the galactosamine (GalN)-sensitized mouse liver after 5 hr. Galactosamine 89-93 tumor necrosis factor Mus musculus 0-21 9742073-1 1998 Tumor necrosis factor (TNF) induces apoptotic death of hepatocytes in the galactosamine (GalN)-sensitized mouse liver after 5 hr. Galactosamine 89-93 tumor necrosis factor Mus musculus 23-26 9657319-7 1998 Therefore, TNF-alpha was suggested to play a critical role on altered expression of constitutive HSC70 and inducible type HSP70 in response of D-galactosamine-sensitized mice to lipopolysaccharide. Galactosamine 143-158 tumor necrosis factor Mus musculus 11-20 9687383-4 1998 Elevated TNF-alpha levels in mice treated with D-galactosamine (GalN)-LPS or GalN-TNF were not reduced by novobiocin; however, the drug exhibited hepatoprotective properties. Galactosamine 47-62 tumor necrosis factor Mus musculus 9-18 9687383-4 1998 Elevated TNF-alpha levels in mice treated with D-galactosamine (GalN)-LPS or GalN-TNF were not reduced by novobiocin; however, the drug exhibited hepatoprotective properties. Galactosamine 47-62 tumor necrosis factor Mus musculus 9-12 9687383-4 1998 Elevated TNF-alpha levels in mice treated with D-galactosamine (GalN)-LPS or GalN-TNF were not reduced by novobiocin; however, the drug exhibited hepatoprotective properties. Galactosamine 64-68 tumor necrosis factor Mus musculus 9-18 9687383-4 1998 Elevated TNF-alpha levels in mice treated with D-galactosamine (GalN)-LPS or GalN-TNF were not reduced by novobiocin; however, the drug exhibited hepatoprotective properties. Galactosamine 64-68 tumor necrosis factor Mus musculus 9-12 9672246-1 1998 Liver injury accompanied by apoptosis of hepatocytes was provoked in mice by an intravenous injection of recombinant tumor necrosis factor-alpha (rTNF-alpha) (1.0 microg/kg) together with an intraperitoneal injection of D-galactosamine (D-gal) (500 mg/kg). Galactosamine 220-235 tumor necrosis factor Mus musculus 117-144 9672246-1 1998 Liver injury accompanied by apoptosis of hepatocytes was provoked in mice by an intravenous injection of recombinant tumor necrosis factor-alpha (rTNF-alpha) (1.0 microg/kg) together with an intraperitoneal injection of D-galactosamine (D-gal) (500 mg/kg). Galactosamine 220-225 tumor necrosis factor Mus musculus 117-144 8879212-4 1996 Furthermore, TNF alpha knockout mice are resistant to the systemic toxicity of LPS upon D-galactosamine sensitization, yet they remain sensitive to high doses of LPS alone. Galactosamine 88-103 tumor necrosis factor Mus musculus 13-22 9426403-4 1997 TNF alpha-deficient mice are resistant to lethal doses of endotoxin and D-galactosamine without hepatocyte apoptosis, yet demonstrate thymus apoptosis. Galactosamine 72-87 tumor necrosis factor Mus musculus 0-9 9317155-1 1997 The acute phase proteins alpha 1-acid glycoprotein (alpha 1-AGP) and alpha 1-antitrypsin (alpha 1-AT) were shown to inhibit, by a mechanism unidentified to date, the lethality induced by TNF both in normal mice and in mice sensitized with galactosamine. Galactosamine 239-252 tumor necrosis factor Mus musculus 187-190 9247576-4 1997 D-Galactosamine (DGalN)-sensitized mice succumb to lethal toxic shock due to macrophage-derived TNF-alpha resulting in fulminant apoptosis of liver cells. Galactosamine 0-15 tumor necrosis factor Mus musculus 96-105 9247576-4 1997 D-Galactosamine (DGalN)-sensitized mice succumb to lethal toxic shock due to macrophage-derived TNF-alpha resulting in fulminant apoptosis of liver cells. Galactosamine 17-22 tumor necrosis factor Mus musculus 96-105 9035283-2 1997 In galactosamine-sensitized C3Heb/FeJ mice, DMSO (10 mL/kg) effectively inhibited endotoxin-induced hepatic NF-kappa B activation, suppressed TNF-alpha levels in plasma by 86%, attenuated intercellular adhesion molecule-1 (ICAM-1) mRNA formation, blocked hepatic neutrophil accumulation by 79%, and reduced liver injury by 80%. Galactosamine 3-16 tumor necrosis factor Mus musculus 142-151 9035283-3 1997 In galactosamine-sensitized mice treated with 20 micrograms/kg murine TNF-alpha, DMSO moderately reduced hepatic NF-kappa B and decreased ICAM-1 mRNA formation and liver injury by 83%, but had no significant effect on hepatic neutrophil accumulation. Galactosamine 3-16 tumor necrosis factor Mus musculus 70-79 8996181-1 1997 Injection of the T cell mitogens concanavalin A (Con A) into nonsensitized or of staphylococcal enterotoxin B (SEB) into D-galactosamine (GalN)-sensitized mice is known to cause fulminant liver failure via a cytokine response syndrome with tumor necrosis factor-alpha (TNF) as the plvotal mediator. Galactosamine 121-136 tumor necrosis factor Mus musculus 240-267 8996181-1 1997 Injection of the T cell mitogens concanavalin A (Con A) into nonsensitized or of staphylococcal enterotoxin B (SEB) into D-galactosamine (GalN)-sensitized mice is known to cause fulminant liver failure via a cytokine response syndrome with tumor necrosis factor-alpha (TNF) as the plvotal mediator. Galactosamine 121-136 tumor necrosis factor Mus musculus 269-272 8780580-1 1996 BACKGROUND & AIMS: Tumor necrosis factor alpha (TNF-alpha) release plays a pivotal role in the pathogenesis of liver injury induced by lipopolysaccharide (LPS) administration in D-galactosamine (GalN)-sensitized mice. Galactosamine 182-197 tumor necrosis factor Mus musculus 23-50 8780580-1 1996 BACKGROUND & AIMS: Tumor necrosis factor alpha (TNF-alpha) release plays a pivotal role in the pathogenesis of liver injury induced by lipopolysaccharide (LPS) administration in D-galactosamine (GalN)-sensitized mice. Galactosamine 182-197 tumor necrosis factor Mus musculus 52-61 8780580-1 1996 BACKGROUND & AIMS: Tumor necrosis factor alpha (TNF-alpha) release plays a pivotal role in the pathogenesis of liver injury induced by lipopolysaccharide (LPS) administration in D-galactosamine (GalN)-sensitized mice. Galactosamine 199-203 tumor necrosis factor Mus musculus 23-50 8780580-1 1996 BACKGROUND & AIMS: Tumor necrosis factor alpha (TNF-alpha) release plays a pivotal role in the pathogenesis of liver injury induced by lipopolysaccharide (LPS) administration in D-galactosamine (GalN)-sensitized mice. Galactosamine 199-203 tumor necrosis factor Mus musculus 52-61 8690213-1 1996 BACKGROUND & AIMS: T cell-dependent liver injury involving endogenous tumor necrosis factor (TNF) alpha can be induced by either concanavalin A in naive mice or by activating anti-CD3 antibody or staphylococcal enterotoxin B in D-galactosamine-sensitized mice. Galactosamine 232-247 tumor necrosis factor Mus musculus 74-107 8613401-0 1996 Streptococcus mitis cell walls and lipopolysaccharide induce lethality in D-galactosamine-sensitized mice by a tumor necrosis factor-dependent pathway. Galactosamine 74-89 tumor necrosis factor Mus musculus 111-132 8764378-6 1996 Moreover, pentoxifylline and A802715 prevented liver injury due to intravenous injection of recombinant TNF in D-galactosamine-sensitized mice. Galactosamine 111-126 tumor necrosis factor Mus musculus 104-107 7622206-10 1995 Injection of DT-5461 2 h before EcLPS challenge prevented the production of serum IL-1 and TNF-alpha in D-galactosamine-treated mice. Galactosamine 104-119 tumor necrosis factor Mus musculus 91-100 8758269-4 1996 The serum total bilirubin (TBIL) and liver necrosis of mice increased more markedly by using of TNF alpha, IL-6 or IFN gamma separately with D-GAL (TBIL: 46.2 +/- 10.6 micromol/L, 44.6 +/- 12.9 micromol/L, 41.9 +/- 14.9 micromol/L), then by D-GAL alone (TBIL: 27 +/- 11 micromol/L) also the serum TBIL of mice and liver necrosis also increased after injection of IL-1, IL-6 with D-GAL and TNF alpha. Galactosamine 141-146 tumor necrosis factor Mus musculus 389-398 8641774-6 1996 Administration of recombinant tumor necrosis factor into D-galactosamine-sensitized mice also caused hepatocyte apoptosis. Galactosamine 57-72 tumor necrosis factor Mus musculus 30-51 8641774-8 1996 It was suggested that lipopolysaccharide- induced hepatic injury and failure in D-galactosamine-sensitized mice was due to the apoptotic cell death of hepatocytes caused by tumor necrosis factor alpha released in the circulation. Galactosamine 80-95 tumor necrosis factor Mus musculus 173-200 8597057-1 1995 D-Galactosamine-sensitized mice challenged with tumor necrosis factor alpha (TNF) developed severe apoptotic and secondary necrotic liver injury as assessed by histology, measurement of cytosolic DNA fragments and determination of liver-specific enzymes in plasma. Galactosamine 0-15 tumor necrosis factor Mus musculus 48-75 8597057-1 1995 D-Galactosamine-sensitized mice challenged with tumor necrosis factor alpha (TNF) developed severe apoptotic and secondary necrotic liver injury as assessed by histology, measurement of cytosolic DNA fragments and determination of liver-specific enzymes in plasma. Galactosamine 0-15 tumor necrosis factor Mus musculus 77-80 7489995-1 1995 Mice sensitized with D-galactosamine (GalN) and challenged with recombinant murine tumor necrosis factor alpha (TNF alpha) developed severe apoptotic and secondary necrotic liver injury as assessed by histology, measurement of cytosolic DNA fragments, and determination of liver specific enzymes in plasma. Galactosamine 21-36 tumor necrosis factor Mus musculus 112-121 7489995-1 1995 Mice sensitized with D-galactosamine (GalN) and challenged with recombinant murine tumor necrosis factor alpha (TNF alpha) developed severe apoptotic and secondary necrotic liver injury as assessed by histology, measurement of cytosolic DNA fragments, and determination of liver specific enzymes in plasma. Galactosamine 38-42 tumor necrosis factor Mus musculus 83-110 8046244-2 1994 However, TNF-alpha induced a concentration-dependent cell death in hepatocytes that had been pretreated with the transcriptional inhibitors actinomycin D (ActD), D-galactosamine, or alpha-amanitin. Galactosamine 162-177 tumor necrosis factor Mus musculus 9-18 7538266-8 1995 TNF-inducible hepatocyte apoptosis in vivo was not only observed in D-galactosamine-sensitized mice, but also when the alternative transcriptional inhibitor actinomycin D was used. Galactosamine 68-83 tumor necrosis factor Mus musculus 0-3 7890366-6 1995 In D-galactosamine-sensitized mice, SEB-induced weight loss but not hypoglycemia was more severe, resulting mostly in death within 24 h. Higher levels of biologically active TNF and IFN-gamma in serum were noted in these mice than in mice receiving SEB only. Galactosamine 3-18 tumor necrosis factor Mus musculus 174-177 7822799-8 1995 We obtained analogous results when we examined the hepatotoxicity of TNF in D-galactosamine-sensitized mice, i.e., DNA fragmentation and liver failure was noted in wild-type mice, whereas TNF-R1-deficient mice were completely resistant. Galactosamine 76-91 tumor necrosis factor Mus musculus 69-72 8844494-0 1995 Platelet-activating factor is a mediator in tumor necrosis factor/galactosamine-induced lethality. Galactosamine 66-79 tumor necrosis factor Mus musculus 44-65 8844494-1 1995 We here report that administration to mice of WEB2170, a potent platelet-activating factor (PAF) receptor antagonist, prevents both PAF-induced and murine tumor necrosis factor (TNF)-induced lethality in galactosamine (GalN)-sensitized mice. Galactosamine 204-217 tumor necrosis factor Mus musculus 155-176 8844494-1 1995 We here report that administration to mice of WEB2170, a potent platelet-activating factor (PAF) receptor antagonist, prevents both PAF-induced and murine tumor necrosis factor (TNF)-induced lethality in galactosamine (GalN)-sensitized mice. Galactosamine 204-217 tumor necrosis factor Mus musculus 178-181 8844494-1 1995 We here report that administration to mice of WEB2170, a potent platelet-activating factor (PAF) receptor antagonist, prevents both PAF-induced and murine tumor necrosis factor (TNF)-induced lethality in galactosamine (GalN)-sensitized mice. Galactosamine 219-223 tumor necrosis factor Mus musculus 155-176 8844494-1 1995 We here report that administration to mice of WEB2170, a potent platelet-activating factor (PAF) receptor antagonist, prevents both PAF-induced and murine tumor necrosis factor (TNF)-induced lethality in galactosamine (GalN)-sensitized mice. Galactosamine 219-223 tumor necrosis factor Mus musculus 178-181 7798795-8 1994 The two lowest concentrations of lipopolysaccharide/galactosamine induced identically low levels of serum TNF, yet in one group all of the animals survived and in the other all died. Galactosamine 52-65 tumor necrosis factor Mus musculus 106-109 7798795-10 1994 GI 147404X, a standard phosphodiesterase type IV inhibitor, inhibited lipopolysaccharide/galactosamine-induced elevation of serum TNF by 90% at doses of 1 and 10 mg/kg. Galactosamine 89-102 tumor necrosis factor Mus musculus 130-133 8245842-3 1993 The envelope fragments exerted lethal effects on mice sensitized with D-galactosamine that were prevented by pretreatment with anti-TNF-alpha serum. Galactosamine 70-85 tumor necrosis factor Mus musculus 132-141 7982269-1 1994 Hydrazine sulfate pretreatment has previously been shown in our laboratory to protect normal mice against endotoxin and D-galactosamine-sensitized mice against both exogenous tumor necrosis factor (TNF) and endotoxin. Galactosamine 120-135 tumor necrosis factor Mus musculus 175-196 7982269-1 1994 Hydrazine sulfate pretreatment has previously been shown in our laboratory to protect normal mice against endotoxin and D-galactosamine-sensitized mice against both exogenous tumor necrosis factor (TNF) and endotoxin. Galactosamine 120-135 tumor necrosis factor Mus musculus 198-201 8299910-6 1994 Passive immunization with anti-TNF-alpha/beta-neutralizing monoclonal antibody (mAb) protected GalN-sensitized mice from the lethal effects of SEB, with less protection with anti-IFN-gamma-neutralizing mAb. Galactosamine 95-99 tumor necrosis factor Mus musculus 31-40 1472981-0 1992 Ornithine and histidine decarboxylase activities in mice sensitized to endotoxin, interleukin-1 or tumour necrosis factor by D-galactosamine. Galactosamine 125-140 tumor necrosis factor Mus musculus 99-121 1335420-1 1992 Oral pretreatment with E3330, a novel quinone derivative, attenuated liver injury induced with tumor necrosis factor-alpha in galactosamine-sensitized mice. Galactosamine 126-139 tumor necrosis factor Mus musculus 95-122 8142601-2 1993 Two animal models, the local Shwartzman reaction and galactosamine (GaLN) induced TNF sensitization, were used. Galactosamine 53-66 tumor necrosis factor Mus musculus 82-85 8142601-2 1993 Two animal models, the local Shwartzman reaction and galactosamine (GaLN) induced TNF sensitization, were used. Galactosamine 68-72 tumor necrosis factor Mus musculus 82-85 1472981-21 1992 These results suggest that suppression of the induction of ODC by GalN may be one cause of the sensitization to LPS, IL-1 or TNF, and that the induction of HDC, i.e. histamine formation, may not be involved in this sensitization.9. Galactosamine 66-70 tumor necrosis factor Mus musculus 125-128 1472981-2 1992 An injection of D-galactosamine (GalN) into mice together with a lipopolysaccharide (LPS or endotoxin), interleukin-1 (IL-1) or tumour necrosis factor (TNF), sensitized the mice and induced fulminant hepatitis with severe congestion resulting in rapid death. Galactosamine 16-31 tumor necrosis factor Mus musculus 128-150 1446388-5 1992 ), delivered 30 min prior to LPS/D-gal, caused a dramatic reduction in serum TNF (40-90%) and protected the animals from the lethal effects of this treatment. Galactosamine 33-38 tumor necrosis factor Mus musculus 77-80 1378868-5 1992 In contrast, when galactosamine-sensitized mice were pretreated with 50 micrograms/kg murine recombinant granulocyte/macrophage CSF instead of G-CSF and subsequently challenged with LPS, serum TNF activity was significantly enhanced and mortality was increased. Galactosamine 18-31 tumor necrosis factor Mus musculus 193-196 1612727-4 1992 Inhibition was apparent in normal and D-galactosamine (GalN)-sensitized mice and occurred at the pretranslational level, as splenic TNF and interleukin-1 beta mRNAs were present in lower amounts in LPS-stimulated mice pretreated with Rs-DPLA. Galactosamine 55-59 tumor necrosis factor Mus musculus 132-135 1612727-5 1992 Consistent with its effects in reducing serum TNF levels, Rs-DPLA pretreatment protected GalN-sensitized mice from a lethal ReLPS challenge. Galactosamine 89-93 tumor necrosis factor Mus musculus 46-49 1727788-7 1992 Furthermore, induction of an a priori acute-phase response protected mice from both D-galactosamine/lipopolysaccharide and D-galactosamine/tumor necrosis factor-alpha-induced death. Galactosamine 123-138 tumor necrosis factor Mus musculus 139-166 1569336-3 1992 In vivo, TNF production was induced in mice treated with D-galactosamine and challenged with LPS. Galactosamine 57-72 tumor necrosis factor Mus musculus 9-12 1563780-1 1992 We have previously shown that malaria parasites liberate exoantigens which, through a phospholipid component, stimulate mouse macrophages to secrete tumor necrosis factor (TNF), which are toxic to D-galactosamine-sensitized mice, and which therefore might be involved in pathology. Galactosamine 197-212 tumor necrosis factor Mus musculus 149-170 1563780-1 1992 We have previously shown that malaria parasites liberate exoantigens which, through a phospholipid component, stimulate mouse macrophages to secrete tumor necrosis factor (TNF), which are toxic to D-galactosamine-sensitized mice, and which therefore might be involved in pathology. Galactosamine 197-212 tumor necrosis factor Mus musculus 172-175 1563785-1 1992 Tumor necrosis factor (TNF) toxicity was induced in vivo by intravenous administration of 15 micrograms of recombinant murine TNF-alpha per kg to galactosamine-sensitized mice. Galactosamine 146-159 tumor necrosis factor Mus musculus 0-21 1563785-1 1992 Tumor necrosis factor (TNF) toxicity was induced in vivo by intravenous administration of 15 micrograms of recombinant murine TNF-alpha per kg to galactosamine-sensitized mice. Galactosamine 146-159 tumor necrosis factor Mus musculus 23-26 1563785-1 1992 Tumor necrosis factor (TNF) toxicity was induced in vivo by intravenous administration of 15 micrograms of recombinant murine TNF-alpha per kg to galactosamine-sensitized mice. Galactosamine 146-159 tumor necrosis factor Mus musculus 126-135 1563785-8 1992 In LPS-responsive NMRI mice which had been protected against galactosamine-LPS-induced hepatitis by pretreatment with colchicine, TNF was still released into the blood. Galactosamine 61-74 tumor necrosis factor Mus musculus 130-133 1727788-9 1992 Thus we suggest that the acute-phase response protects against death in D-galactosamine-sensitized mice through an interaction with mediators of shock subsequent to tumor necrosis factor-alpha release. Galactosamine 72-87 tumor necrosis factor Mus musculus 165-192 1798293-2 1991 As a model for organ failure in septic shock, three alternative experimental approaches with a common pathology are presented: When galactosamine-sensitized mice receive either lipopolysaccharide or leukotriene D4 or tumor necrosis factor alpha they develop fulminant hepatitis within few hours with a lethal outcome within one day. Galactosamine 132-145 tumor necrosis factor Mus musculus 199-244 1537589-2 1992 Blood-stage parasites of human and rodent malarial parasites release serologically related exoantigens which induce the production of TNF in vitro and in vivo and which can kill mice made hypersensitive to TNF by pretreatment with D-galactosamine. Galactosamine 231-246 tumor necrosis factor Mus musculus 206-209 2654012-6 1989 Mice made hypersensitive to the lethal action of TNF by pretreatment with D-galactosamine were killed in a dose-related fashion by administration of antigen preparations; addition of specific antiserum or prior vaccination with the antigens protected such mice, but not those given LPS, from death. Galactosamine 74-89 tumor necrosis factor Mus musculus 49-52 1657127-1 1991 In this study, we investigated the influence of D-galactosamine (GalN), indomethacin, and dexamethasone on the pharmacokinetics of injected or induced tumor necrosis factor (TNF) and interleukin-6 (IL-6) after a bolus injection of murine TNF (mTNF) or lipopolysaccharide (LPS). Galactosamine 48-63 tumor necrosis factor Mus musculus 151-172 1657127-1 1991 In this study, we investigated the influence of D-galactosamine (GalN), indomethacin, and dexamethasone on the pharmacokinetics of injected or induced tumor necrosis factor (TNF) and interleukin-6 (IL-6) after a bolus injection of murine TNF (mTNF) or lipopolysaccharide (LPS). Galactosamine 65-69 tumor necrosis factor Mus musculus 151-172 1657127-1 1991 In this study, we investigated the influence of D-galactosamine (GalN), indomethacin, and dexamethasone on the pharmacokinetics of injected or induced tumor necrosis factor (TNF) and interleukin-6 (IL-6) after a bolus injection of murine TNF (mTNF) or lipopolysaccharide (LPS). Galactosamine 65-69 tumor necrosis factor Mus musculus 174-177 2227817-0 1990 Involvement of tumor necrosis factor-alpha in development of hepatic injury in galactosamine-sensitized mice. Galactosamine 79-92 tumor necrosis factor Mus musculus 15-42 2400992-1 1990 Both recombinant tumor necrosis factor (rTNF) and recombinant interleukin 1 (rIL-1) are able to mediate vascular collapse and death in a previously described murine model, using galactosamine to enhance the toxicity of these cytokines. Galactosamine 178-191 tumor necrosis factor Mus musculus 17-38 2344657-6 1990 POF was found to inhibit the appearance of TNF in serum of LPS-treated, D-galactosamine-sensitized mice and in the supernatants of LPS-stimulated, thioglycollate-induced mouse peritoneal macrophages. Galactosamine 72-87 tumor necrosis factor Mus musculus 43-46 2674557-2 1989 We have shown that human and rodent blood-stage parasites liberate heat-stable soluble antigens that induce the release of TNF by activated macrophages in vitro and in vivo, and are toxic to mice made hypersensitive to TNF by D-galactosamine. Galactosamine 226-241 tumor necrosis factor Mus musculus 219-222 1716205-11 1991 Finally, prophylactic administration of a monoclonal antibody against murine TNF protected normal and galactosamine-sensitized mice from a lethal dose of LPS and yet had no protective effect in adrex animals. Galactosamine 102-115 tumor necrosis factor Mus musculus 77-80 1657127-8 1991 We conclude that the strongly enhanced sensitivity of GalN-treated mice towards mTNF-induced or LPS-induced lethality was not reflected in circulating TNF or IL-6 levels, and that dexamethasone and indomethacin both reduce circulating IL-6 concentrations in mice treated with TNF and LPS. Galactosamine 54-58 tumor necrosis factor Mus musculus 81-84 1932370-4 1991 Using adrenalectomized mice, which are less sensitive to LPS toxicity than galactosamine-treated mice, it was shown that smaller doses of LPS were effective in inducing TNF release in comparison with intact animals, and that larger concentrations of serum TNF were obtained. Galactosamine 75-88 tumor necrosis factor Mus musculus 169-172 1932370-4 1991 Using adrenalectomized mice, which are less sensitive to LPS toxicity than galactosamine-treated mice, it was shown that smaller doses of LPS were effective in inducing TNF release in comparison with intact animals, and that larger concentrations of serum TNF were obtained. Galactosamine 75-88 tumor necrosis factor Mus musculus 256-259 2037372-0 1991 Tumor necrosis factor alpha mediates lethal activity of killed gram-negative and gram-positive bacteria in D-galactosamine-treated mice. Galactosamine 107-122 tumor necrosis factor Mus musculus 0-27 1988538-16 1991 Hydrazine sulfate pretreatment also protects D-galactosamine-sensitized mice against the lethal effects of injected tumor necrosis factor/cachectin. Galactosamine 45-60 tumor necrosis factor Mus musculus 138-147 1774433-0 1991 Interleukin-1 alpha enhances hepatotoxicity of tumor necrosis factor-alpha in galactosamine-sensitized mice. Galactosamine 78-91 tumor necrosis factor Mus musculus 47-74 1774433-5 1991 However, recombinant murine IL-1 alpha enhanced the hepatotoxic effect of recombinant murine TNF in galactosamine-sensitized mice. Galactosamine 100-113 tumor necrosis factor Mus musculus 93-96 2403385-20 1990 We conclude from our findings that changes in leukocyte numbers and composition following D-galactosamine LPS or D-galactosamine/TNF alpha administration is an epiphenomenon rather than a causal event of leukocyte stimulation in the process of inducing a fulminant hepatitis in mice. Galactosamine 113-128 tumor necrosis factor Mus musculus 129-138 16530740-3 2006 Inhibitory doses (ID(50)) of compounds 12, 17b, 19a, and 19b on TNFalpha production induced by co-injection of galactosamine and LPS in C3H/HeN mice in vivo were measured. Galactosamine 111-124 tumor necrosis factor Mus musculus 64-72 3819645-0 1987 Lethal toxicity of lipopolysaccharide and tumor necrosis factor in normal and D-galactosamine-treated mice. Galactosamine 78-93 tumor necrosis factor Mus musculus 42-63 2465008-0 1989 Tumor necrosis factor is a terminal mediator in galactosamine/endotoxin-induced hepatitis in mice. Galactosamine 48-61 tumor necrosis factor Mus musculus 0-21 2465008-1 1989 Intravenous injection of murine recombinant tumor necrosis factor alpha(TNF-alpha) to male NMRI albino mice in doses greater than 4 micrograms/kg (specific activity 4 x 10(7) U/mg) resulted in a fulminant hepatitis when animals had been sensitized 1 hr before by intraperitoneal administration of 700 mg/kg galactosamine. Galactosamine 307-320 tumor necrosis factor Mus musculus 44-71 2465008-1 1989 Intravenous injection of murine recombinant tumor necrosis factor alpha(TNF-alpha) to male NMRI albino mice in doses greater than 4 micrograms/kg (specific activity 4 x 10(7) U/mg) resulted in a fulminant hepatitis when animals had been sensitized 1 hr before by intraperitoneal administration of 700 mg/kg galactosamine. Galactosamine 307-320 tumor necrosis factor Mus musculus 72-81 3192926-7 1988 This reflects the well-known D-galactosamine sensitization against lipopolysaccharide or TNF. Galactosamine 29-44 tumor necrosis factor Mus musculus 89-92 3819645-2 1987 C3H/TifF mice treated with D-galactosamine were rendered sensitive to the lethal effects of submicrogram amounts of TNF. Galactosamine 27-42 tumor necrosis factor Mus musculus 116-119 3819645-4 1987 The duration of sensitization to TNF lasted up to 8 h after D-galactosamine administration, that towards LPS, up to 4 h. As with LPS, with TNF sensitization could be inhibited by uridine administered up to 2 h after D-galactosamine/TNF, showing that the early biochemical alterations in the liver known to be necessary for sensitization to LPS are also necessary for sensitization to TNF. Galactosamine 60-75 tumor necrosis factor Mus musculus 33-36 3819645-4 1987 The duration of sensitization to TNF lasted up to 8 h after D-galactosamine administration, that towards LPS, up to 4 h. As with LPS, with TNF sensitization could be inhibited by uridine administered up to 2 h after D-galactosamine/TNF, showing that the early biochemical alterations in the liver known to be necessary for sensitization to LPS are also necessary for sensitization to TNF. Galactosamine 216-231 tumor necrosis factor Mus musculus 33-36 3819645-4 1987 The duration of sensitization to TNF lasted up to 8 h after D-galactosamine administration, that towards LPS, up to 4 h. As with LPS, with TNF sensitization could be inhibited by uridine administered up to 2 h after D-galactosamine/TNF, showing that the early biochemical alterations in the liver known to be necessary for sensitization to LPS are also necessary for sensitization to TNF. Galactosamine 216-231 tumor necrosis factor Mus musculus 139-142 3819645-4 1987 The duration of sensitization to TNF lasted up to 8 h after D-galactosamine administration, that towards LPS, up to 4 h. As with LPS, with TNF sensitization could be inhibited by uridine administered up to 2 h after D-galactosamine/TNF, showing that the early biochemical alterations in the liver known to be necessary for sensitization to LPS are also necessary for sensitization to TNF. Galactosamine 216-231 tumor necrosis factor Mus musculus 139-142 3819645-4 1987 The duration of sensitization to TNF lasted up to 8 h after D-galactosamine administration, that towards LPS, up to 4 h. As with LPS, with TNF sensitization could be inhibited by uridine administered up to 2 h after D-galactosamine/TNF, showing that the early biochemical alterations in the liver known to be necessary for sensitization to LPS are also necessary for sensitization to TNF. Galactosamine 216-231 tumor necrosis factor Mus musculus 139-142 3819645-5 1987 In contrast to LPS, the toxicity of TNF was expressed also in D-galactosamine-treated endotoxin-resistant C3H/HeJ mice. Galactosamine 62-77 tumor necrosis factor Mus musculus 36-39