PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 22963044-0 2012 Pretreatment of hepatocyte growth factor gene transfer mediated by octaarginine peptide-modified nanoparticles ameliorates LPS/D-galactosamine-induced hepatitis. Galactosamine 127-142 toll-like receptor 4 Mus musculus 123-126 22963044-2 2012 In this study, we report on an examination of whether this gene delivery system exerts potent hepatoprotective effects against lipopolysaccharide/D-galactosamine (LPS/D-GalN)-induced acute liver injury. Galactosamine 146-161 toll-like receptor 4 Mus musculus 163-166 22415073-0 2012 Reduced hepatic injury in Toll-like receptor 4-deficient mice following D-galactosamine/lipopolysaccharide-induced fulminant hepatic failure. Galactosamine 72-87 toll-like receptor 4 Mus musculus 26-46 22415073-4 2012 The aim of this study was to investigate the role of TLR4 in FHF induced by D-GalN/LPS administration in mice. Galactosamine 76-82 toll-like receptor 4 Mus musculus 53-57 19818826-5 2010 GalN/LPS increased the mortality and serum aminotransferase activities. Galactosamine 0-4 toll-like receptor 4 Mus musculus 5-8 19997066-4 2010 LPS/GalN-treated PXR-null mice had greater increases of alanine transaminase (ALT), hepatocyte apoptosis, necrosis, and hemorrhagic liver injury than wild-type mice. Galactosamine 4-8 toll-like receptor 4 Mus musculus 0-3 19997066-5 2010 LPS/GalN-mediated phosphorylation of JNK1/2 and ERK1/2 was differentially regulated in wild-type and PXR-null mice. Galactosamine 4-8 toll-like receptor 4 Mus musculus 0-3 19997066-6 2010 Importantly, LPS/GalN-induced hepatic Stat3 survival signaling was impaired and early activation of Jak2 was delayed in PXR-null mice. Galactosamine 17-21 toll-like receptor 4 Mus musculus 13-16 19997066-12 2010 Increases of LPS/GalN-induced hepatocyte apoptosis and liver injury in PXR-null mice are due to deregulated mitogen-activated protein (MAP) kinase activation as well as delayed Jak2/Stat3 activation, which lead to a compromise in defense mechanisms that involve Bcl-xL-, HO-1, and autophagy-mediated pathways. Galactosamine 17-21 toll-like receptor 4 Mus musculus 13-16 21835267-5 2011 Furthermore, CTN significantly increased the survival rate against LPS challenge in D-galactosamine-sensitized mice, which was in line with in vitro results. Galactosamine 84-99 toll-like receptor 4 Mus musculus 67-70 19818826-7 2010 GalN/LPS increased hepatic lipid peroxidation and decreased the contents of reduced glutathione. Galactosamine 0-4 toll-like receptor 4 Mus musculus 5-8 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 toll-like receptor 4 Mus musculus 5-8 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 toll-like receptor 4 Mus musculus 5-8 19682082-10 2009 Glutathione-S-transferase (GST) activity was stimulated by LPS/D-GalN exposure and p-methoxyl-diphenyl diselenide, at all doses, protected against this alteration. Galactosamine 63-69 toll-like receptor 4 Mus musculus 59-62 19682082-11 2009 p-Methoxyl-diphenyl diselenide was effective in ameliorating inhibition of catalase activity induced by LPS/d-GalN exposure. Galactosamine 108-114 toll-like receptor 4 Mus musculus 104-107 19682082-13 2009 p-Methoxyl-diphenyl diselenide significantly attenuated LPS/D-GalN-induced hepatic histopathological alterations. Galactosamine 60-66 toll-like receptor 4 Mus musculus 56-59 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 toll-like receptor 4 Mus musculus 193-196 19852690-7 2009 Analysis of intravital fluorescence microscopy revealed that LPS/D-gal caused a strong inflammatory reaction of the venous endothelium with significant induction of platelet and leukocyte tethering, rolling and adhesion. Galactosamine 65-70 toll-like receptor 4 Mus musculus 61-64 19852690-8 2009 Secondary interactions of platelets to adherent or rolling platelets or leukocytes were also increased after LPS/D-gal-injection. Galactosamine 113-118 toll-like receptor 4 Mus musculus 109-112 20157398-3 2008 Intra-peritoneal pretreatment of mice with decursinol (50 mg/kg) markedly enhanced the LPS/GalN-induced increase of plasma interleukin-10 (IL-10) levels, without affecting plasma TNF-alpha, IL-6 and IL-12 levels. Galactosamine 91-95 toll-like receptor 4 Mus musculus 87-90 18251086-10 2008 The results indicated that MMP-9 played a role in the development of LPS/GalN- induced mouse liver injury, and suggested that an inhibition by glycyrrhizin of the acute liver injury may have been due to a down-regulation of MMP-9. Galactosamine 73-77 toll-like receptor 4 Mus musculus 69-72 17911593-9 2007 Finally, Emu-miR-155 transgenic mice produced higher levels of TNF-alpha when exposed to LPS and were hypersensitive to LPS/d-galactosamine-induced septic shock. Galactosamine 126-139 toll-like receptor 4 Mus musculus 120-123 17151479-5 2006 All the mice injected intraperitoneally with LPS and D-galactosamine (LPS+GalN) died within 24 h. However, a peritoneal injection, but no intravenous or oral administration, of SCE (500-1,000 mg/kg) at 3 to 48 h before the LPS+GalN-challenge resulted in a significantly improved survival rate. Galactosamine 53-68 toll-like receptor 4 Mus musculus 70-73 17151479-5 2006 All the mice injected intraperitoneally with LPS and D-galactosamine (LPS+GalN) died within 24 h. However, a peritoneal injection, but no intravenous or oral administration, of SCE (500-1,000 mg/kg) at 3 to 48 h before the LPS+GalN-challenge resulted in a significantly improved survival rate. Galactosamine 53-68 toll-like receptor 4 Mus musculus 70-73 17353199-8 2007 d-Galactosamine-sensitized mice expressing defective TLR4 or lacking TLR4 expression acquired susceptibility to eLPS-driven toxemia upon IFNgamma priming, whereas double deficient mice did not. Galactosamine 0-15 toll-like receptor 4 Mus musculus 53-57 17353199-8 2007 d-Galactosamine-sensitized mice expressing defective TLR4 or lacking TLR4 expression acquired susceptibility to eLPS-driven toxemia upon IFNgamma priming, whereas double deficient mice did not. Galactosamine 0-15 toll-like receptor 4 Mus musculus 69-73 16547261-3 2006 In this study, we show that a mAb to TLR4/MD-2 protected mice from acute lethal hepatitis caused by LPS/d-galactosamine. Galactosamine 104-119 toll-like receptor 4 Mus musculus 37-41 16547261-6 2006 These results demonstrated that an agonistic mAb to TLR4/MD-2 protected mice from LPS/d-galactosamine-induced acute lethal hepatitis by delivering a protective signal activating NF-kappaB through TLR4/MD-2. Galactosamine 88-101 toll-like receptor 4 Mus musculus 52-56 16547261-6 2006 These results demonstrated that an agonistic mAb to TLR4/MD-2 protected mice from LPS/d-galactosamine-induced acute lethal hepatitis by delivering a protective signal activating NF-kappaB through TLR4/MD-2. Galactosamine 88-101 toll-like receptor 4 Mus musculus 196-200 16051691-3 2005 Pretreatment with histamine ameliorated the GalN/LPS-induced necrotic and apoptotic changes in the hepatocytes and inhibited the elevation of serum AST and ALT levels. Galactosamine 44-48 toll-like receptor 4 Mus musculus 49-52 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 toll-like receptor 4 Mus musculus 30-33 16051691-5 2005 Histamine inhibited the GalN/LPS-induced caspase-3 activity in the liver. Galactosamine 24-28 toll-like receptor 4 Mus musculus 29-32 11748185-5 2002 In contrast, infection with live T. pectinovorum induced 100% lethality within 12 h in GalN-sensitized LPS responder mice, indicating an endotoxin-like property of this treponeme. Galactosamine 87-91 toll-like receptor 4 Mus musculus 103-106 15387909-9 2004 The mortality reached up to 80% at 10 h. TLR2 mRNA was expressed at a low level in liver tissues of normal mice, while it was significantly increased and maintained at a higher level following intraperitoneal injection with D-Gal/LPS. Galactosamine 224-229 toll-like receptor 4 Mus musculus 230-233 12963146-3 2003 The effect of the extract on lipopolysaccharide (LPS)-induced septic shock was evaluated by measuring the number of deaths and the levels of serum alanine and aspartate aminotransferases following intraperitoneal injection of LPS (1 microg/kg) into D-galactosamine-primed mice. Galactosamine 249-264 toll-like receptor 4 Mus musculus 49-52 15850520-2 2005 METHODS: Liver damage was induced by lipopolysaccharide (LPS)/TNFalpha in D-galactosamine (GalN) sensitized BALB/c mice. Galactosamine 74-89 toll-like receptor 4 Mus musculus 57-60 15577225-4 2004 Pretreatment of animals with protocatechuic acid effectively suppressed LPS/GalN-induced lethality; protocatechuic acid isopropyl ester was the most effective among the various derivatives of protocatechuic acid. Galactosamine 76-80 toll-like receptor 4 Mus musculus 72-75 15577225-6 2004 Pretreatment with protocatechuic acid isopropyl ester effectively suppressed the LPS/GalN-induced increase in plasma tumor necrosis factor (TNF)-alpha alanine aminotransferase (ALT), nitrite/nitrate levels, and hepatic malondialdehyde levels. Galactosamine 85-89 toll-like receptor 4 Mus musculus 81-84 15577225-7 2004 In contrast, it markedly enhanced the LPS/GalN-induced increase in plasma interleukin (IL)-10 levels, without any changes in IL-6 plasma levels. Galactosamine 42-46 toll-like receptor 4 Mus musculus 38-41 11740732-7 2001 In galactosamine-treated mice, the minimum ig dose of LPS needed to induce lethal hepatitis was very small (less than that needed by ip injection). Galactosamine 3-16 toll-like receptor 4 Mus musculus 54-57 1934597-1 1991 The antitumour antibiotic actinomycin D (Act D) and the aminosugar D-galactosamine both enhance the sensitivity of animals to bacterial lipopolysaccharide (LPS). Galactosamine 67-82 toll-like receptor 4 Mus musculus 156-159 10498828-0 1999 Enhancement by galactosamine of lipopolysaccharide(LPS)-induced tumour necrosis factor production and lethality: its suppression by LPS pretreatment. Galactosamine 15-28 toll-like receptor 4 Mus musculus 51-54 10498828-0 1999 Enhancement by galactosamine of lipopolysaccharide(LPS)-induced tumour necrosis factor production and lethality: its suppression by LPS pretreatment. Galactosamine 15-28 toll-like receptor 4 Mus musculus 132-135 10498828-3 1999 Co-injection of GalN and lipopolysaccharide (LPS) into mice produces fulminant hepatitis with severe hepatic congestion, resulting in rapid death. Galactosamine 16-20 toll-like receptor 4 Mus musculus 45-48 10498828-5 1999 Administration of uridine (a precursor of UTP) prior injection of either LPS itself or interleukin-1 (IL-1) reduces the lethality of GalN+LPS. Galactosamine 133-137 toll-like receptor 4 Mus musculus 73-76 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 toll-like receptor 4 Mus musculus 11-14 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 toll-like receptor 4 Mus musculus 177-180 9573062-2 1998 The present study examined the protective effect of a synthetic 27-amino-acid peptide (CAP18(109-135)) from the LPS-binding domain of CAP18 against antibiotic-induced endotoxin shock, using highly LPS-sensitive D-(+)-galactosamine (D-GalN)-sensitized C3H/HeN mice. Galactosamine 211-230 toll-like receptor 4 Mus musculus 197-200 7520172-2 1994 In a previous study, polyclonal anti-LBP IgGs were found to protect D-galactosamine-sensitized mice against a lethal endotoxemic shock induced by a low challenge of LPS or lipid A when administered simultaneously with endotoxin. Galactosamine 68-83 toll-like receptor 4 Mus musculus 165-168 8418160-1 1993 A radiolabeled lipopolysaccharide (LPS) from Salmonella choleraesuis was as toxic for galactosamine-treated mice as the unlabeled preparation. Galactosamine 86-99 toll-like receptor 4 Mus musculus 35-38 7806345-7 1995 However, two hydrophilic derivatives with low activity as priming agents were capable of decreasing the toxicity of LPS when given after the challenge in galactosamine-sensitized mice. Galactosamine 154-167 toll-like receptor 4 Mus musculus 116-119 7927709-2 1994 On the basis of LPS-induced spleen cell mitogenesis, macrophage tumor necrosis factor secretion, and tyrosine phosphorylation in vitro and lethality in galactosamine-sensitized mice in vivo, the C.C3H-Lpsd strain provides a model of LPS hyporesponsiveness that is comparable to that of the parental C3H/HeJ strain. Galactosamine 152-165 toll-like receptor 4 Mus musculus 16-19 8168521-3 1994 Synthetic lipid A analogues with monosaccharide backbones, GLA-60, GLA-69 and GLA-58, which exhibit potent, weak and scarce agonistic activities of LPS, respectively, induced tolerance against LPS lethality in galactosamine-(GalN)-sensitized mice while none of them were pyrogenic in rabbits. Galactosamine 210-223 toll-like receptor 4 Mus musculus 148-151 8168521-3 1994 Synthetic lipid A analogues with monosaccharide backbones, GLA-60, GLA-69 and GLA-58, which exhibit potent, weak and scarce agonistic activities of LPS, respectively, induced tolerance against LPS lethality in galactosamine-(GalN)-sensitized mice while none of them were pyrogenic in rabbits. Galactosamine 210-223 toll-like receptor 4 Mus musculus 193-196 31868940-5 2020 Camp deficiency exacerbated LPS-induced myocardial depression, while the administration of CRAMP (the mature form of mouse cathelicidin) decreased the LPS-induced mortality in a D-galactosamine hydrochloride (D-GalN)-sensitized endotoxin shock model. Galactosamine 178-207 toll-like receptor 4 Mus musculus 151-154 1716205-8 1991 LPS tolerance was also investigated in the galactosamine LPS model which like the adrex model is characterized by a thousandfold increase in the sensitivity of these animals to the lethal effects of LPS. Galactosamine 43-56 toll-like receptor 4 Mus musculus 0-3 1716205-8 1991 LPS tolerance was also investigated in the galactosamine LPS model which like the adrex model is characterized by a thousandfold increase in the sensitivity of these animals to the lethal effects of LPS. Galactosamine 43-56 toll-like receptor 4 Mus musculus 57-60 1716205-8 1991 LPS tolerance was also investigated in the galactosamine LPS model which like the adrex model is characterized by a thousandfold increase in the sensitivity of these animals to the lethal effects of LPS. Galactosamine 43-56 toll-like receptor 4 Mus musculus 57-60 1716205-9 1991 Consistent with the absence of LPS tolerance in adrex mice, galactosamine-sensitized mice were also responsive to a second LPS stimulus and did not become LPS tolerant. Galactosamine 60-73 toll-like receptor 4 Mus musculus 123-126 1716205-9 1991 Consistent with the absence of LPS tolerance in adrex mice, galactosamine-sensitized mice were also responsive to a second LPS stimulus and did not become LPS tolerant. Galactosamine 60-73 toll-like receptor 4 Mus musculus 123-126 1716205-10 1991 While LPS-treated adrex mice had no significant increases in serum corticosterone, corticosterone levels in LPS-treated galactosamine-sensitized mice were comparable to LPS-stimulated normals suggesting that LPS tolerance involves both glucocorticoid-dependent and -independent components. Galactosamine 120-133 toll-like receptor 4 Mus musculus 108-111 1716205-10 1991 While LPS-treated adrex mice had no significant increases in serum corticosterone, corticosterone levels in LPS-treated galactosamine-sensitized mice were comparable to LPS-stimulated normals suggesting that LPS tolerance involves both glucocorticoid-dependent and -independent components. Galactosamine 120-133 toll-like receptor 4 Mus musculus 108-111 1716205-10 1991 While LPS-treated adrex mice had no significant increases in serum corticosterone, corticosterone levels in LPS-treated galactosamine-sensitized mice were comparable to LPS-stimulated normals suggesting that LPS tolerance involves both glucocorticoid-dependent and -independent components. Galactosamine 120-133 toll-like receptor 4 Mus musculus 108-111 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 toll-like receptor 4 Mus musculus 154-157 2228245-5 1990 LPS from the phototrophic strain Rhodobacter capsulatus 37b4 elaborated little toxicity in galactosamine-treated mice (10 micrograms of LPS per mouse was the 100% lethal dose [LD100]) and induced IL-1 and IL-6 release only at high concentrations (10 to 50 micrograms of LPS per ml). Galactosamine 91-104 toll-like receptor 4 Mus musculus 0-3 2037372-1 1991 Treatment with D-galactosamine increases sensitivity of lipopolysaccharide (LPS)-responder mice to the lethal effects of LPS, while nonresponder mice remain resistant (M.A. Galactosamine 15-30 toll-like receptor 4 Mus musculus 76-79 2037372-1 1991 Treatment with D-galactosamine increases sensitivity of lipopolysaccharide (LPS)-responder mice to the lethal effects of LPS, while nonresponder mice remain resistant (M.A. Galactosamine 15-30 toll-like receptor 4 Mus musculus 121-124 2037372-5 1991 In the present study it is shown that, in contrast to LPS, killed gram-negative bacteria (Salmonella abortus equi and S. typhimurium) were highly toxic for D-galactosamine-treated LPS-responder (C57BL/10 ScSN and C3H/HeN) and -nonresponder (C57BL/10 ScCR and C3H/HeJ) mice, although to a higher extent in the former strains. Galactosamine 156-171 toll-like receptor 4 Mus musculus 180-183 3356468-0 1988 Induction of tolerance to lipopolysaccharide (LPS)-D-galactosamine lethality by pretreatment with LPS is mediated by macrophages. Galactosamine 53-66 toll-like receptor 4 Mus musculus 46-49 3356468-0 1988 Induction of tolerance to lipopolysaccharide (LPS)-D-galactosamine lethality by pretreatment with LPS is mediated by macrophages. Galactosamine 53-66 toll-like receptor 4 Mus musculus 98-101 3356468-1 1988 In mice treated with D-galactosamine, lipopolysaccharide (LPS) exhibits enhanced toxicity (C. Galanos, M. A. Freudenberg, and W. Reutter, Proc. Galactosamine 21-36 toll-like receptor 4 Mus musculus 58-61 3356468-6 1988 Pretreatment of mice with LPS before D-galactosamine rendered them tolerant to the enhanced lethal effect of LPS. Galactosamine 37-52 toll-like receptor 4 Mus musculus 26-29 3356468-12 1988 C3H/HeN macrophages (2 X 10(7], incubated with minute amounts of LPS (0.5 to 0.02 microgram) in vitro and transferred subsequently to C3H/HeJ mice, induced lethality when administered together with or after D-galactosamine and tolerance when injected before D-galactosamine. Galactosamine 207-222 toll-like receptor 4 Mus musculus 65-68 3356468-12 1988 C3H/HeN macrophages (2 X 10(7], incubated with minute amounts of LPS (0.5 to 0.02 microgram) in vitro and transferred subsequently to C3H/HeJ mice, induced lethality when administered together with or after D-galactosamine and tolerance when injected before D-galactosamine. Galactosamine 258-273 toll-like receptor 4 Mus musculus 65-68 33083887-2 2021 The purpose of this study was to determine the protective effect of the Toll-like receptor 4 (TLR4) inhibitor TAK-242 on lipopolysaccharide (LPS)/D-galactosamine (D-GalN)-induced explosive hepatitis and explore in vivo and in vitro mechanisms. Galactosamine 146-161 toll-like receptor 4 Mus musculus 72-92 33083887-2 2021 The purpose of this study was to determine the protective effect of the Toll-like receptor 4 (TLR4) inhibitor TAK-242 on lipopolysaccharide (LPS)/D-galactosamine (D-GalN)-induced explosive hepatitis and explore in vivo and in vitro mechanisms. Galactosamine 146-161 toll-like receptor 4 Mus musculus 94-98 33083887-2 2021 The purpose of this study was to determine the protective effect of the Toll-like receptor 4 (TLR4) inhibitor TAK-242 on lipopolysaccharide (LPS)/D-galactosamine (D-GalN)-induced explosive hepatitis and explore in vivo and in vitro mechanisms. Galactosamine 163-169 toll-like receptor 4 Mus musculus 72-92 33083887-2 2021 The purpose of this study was to determine the protective effect of the Toll-like receptor 4 (TLR4) inhibitor TAK-242 on lipopolysaccharide (LPS)/D-galactosamine (D-GalN)-induced explosive hepatitis and explore in vivo and in vitro mechanisms. Galactosamine 163-169 toll-like receptor 4 Mus musculus 94-98 31474165-0 2019 Succinate dehydrogenase inhibitor dimethyl malonate alleviates LPS/d-galactosamine-induced acute hepatic damage in mice. Galactosamine 67-82 toll-like receptor 4 Mus musculus 63-66 29057809-8 2017 Furthermore, KAR inhibits the apoptosis of hepatocytes and reduces the expression of TLR4 and NF-kappaB signaling pathway-related proteins induced by GalN/LPS treatment. Galactosamine 150-154 toll-like receptor 4 Mus musculus 85-89 31074668-0 2019 Pretreatment with Salvia miltiorrhiza Polysaccharides Protects from Lipopolysaccharides/d-Galactosamine-Induced Liver Injury in Mice Through Inhibiting TLR4/MyD88 Signaling Pathway. Galactosamine 88-103 toll-like receptor 4 Mus musculus 152-156 31077206-0 2019 Apolipoprotein A5 alleviates LPS/D-GalN-induced fulminant liver failure in mice by inhibiting TLR4-mediated NF-kappaB pathway. Galactosamine 35-39 toll-like receptor 4 Mus musculus 29-32 31077206-0 2019 Apolipoprotein A5 alleviates LPS/D-GalN-induced fulminant liver failure in mice by inhibiting TLR4-mediated NF-kappaB pathway. Galactosamine 35-39 toll-like receptor 4 Mus musculus 94-98 31077206-18 2019 CONCLUSION: ApoA5 had a protective effect against LPS/D-GalN-induced fulminant liver failure in mice within a certain range by inhibiting TLR4-mediated NF-kappaB pathway. Galactosamine 56-60 toll-like receptor 4 Mus musculus 138-142 28963941-2 2017 However, the underlying mechanism of how quercetin to protect against lipopolysaccharides/d-galactosamine (LPS/d-GalN) induced acute liver injury remains unclear. Galactosamine 90-105 toll-like receptor 4 Mus musculus 107-110 28887131-3 2017 Acute liver injury was induced by lipopolysaccharide/d-galactosamine (LPS/GalN) in mice. Galactosamine 53-68 toll-like receptor 4 Mus musculus 70-73 27670746-7 2016 Using a murine LPS/D-galactosamine endotoxaemia model we showed that treatment with B. quintana LPS could improve the survival rate significantly. Galactosamine 21-34 toll-like receptor 4 Mus musculus 96-99 28213269-0 2017 Protective effects of morin on lipopolysaccharide/d-galactosamine-induced acute liver injury by inhibiting TLR4/NF-kappaB and activating Nrf2/HO-1 signaling pathways. Galactosamine 50-65 toll-like receptor 4 Mus musculus 107-111 27711079-3 2016 Ablation of Sirt1 shows remarkable protection against GalN/LPS-induced liver injury, which is a result of enhanced NF-kappaB response because knockdown of RelA/p65 negates the protective effect of Sirt1 knockout. Galactosamine 54-58 toll-like receptor 4 Mus musculus 59-62 26494508-0 2015 Protective effects of sea buckthorn polysaccharide extracts against LPS/d-GalN-induced acute liver failure in mice via suppressing TLR4-NF-kappaB signaling. Galactosamine 72-78 toll-like receptor 4 Mus musculus 131-135 27627914-7 2016 Additionally, these results highlighted the hepatoprotective and curative effects of Xs-ME in a mouse model of LPS/D-GalN-induced acute liver injury, as assessed by elevated serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT), and histological damage. Galactosamine 117-121 toll-like receptor 4 Mus musculus 111-114 26494508-12 2015 CONCLUSIONS: This study indicates that pretreatment with HRP protects against LPS/d-GalN-induced liver injury in mice via suppressing the TLR4-NF-kappaB signaling pathway. Galactosamine 82-88 toll-like receptor 4 Mus musculus 138-142 25173984-0 2014 Emodin ameliorated lipopolysaccharide-induced fulminant hepatic failure by blockade of TLR4/MD2 complex expression in D-galactosamine-sensitized mice. Galactosamine 118-133 toll-like receptor 4 Mus musculus 87-91 25382719-9 2014 These findings suggest that 1 protects against GalN/LPS-induced liver injury by suppressing TLR4 signaling and enhancing autophagic flux. Galactosamine 47-51 toll-like receptor 4 Mus musculus 92-96 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 toll-like receptor 4 Mus musculus 85-88 25749929-11 2015 Together, these data are the first to demonstrate that CB2 activation attenuates GalN/LPS-induced ALF by inducing an M1 to M2 shift in macrophages and by regulating the expression of unique miRs that target key molecules involved in the TLR4 pathway. Galactosamine 81-85 toll-like receptor 4 Mus musculus 237-241 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 toll-like receptor 4 Mus musculus 20-23 25325613-7 2014 Interestingly, 1 augmented GalN/LPS-mediated increases in the protein expression of IRAK-M, a negative regulator of TLR signaling. Galactosamine 27-31 toll-like receptor 4 Mus musculus 32-35 24895481-7 2014 Furthermore, treatment with galactosamine/lipopolysaccharide markedly increased toll-like receptor 4, nuclear level of nuclear factor-kappaB, and phosphorylation of both extracellular signal-regulated kinase and c-Jun N-terminal kinase in liver tissues. Galactosamine 28-41 toll-like receptor 4 Mus musculus 80-100