D(+)-Galactosamine hydrochloride, a well-known experimental toxin, primarily inflicts liver damage through free radical production and UTP nucleotide depletion. Intoxication with D(+)-Galactosamine hydrochloride also leads to renal dysfunction, often culminating in renal failure associated with severe liver damage. The combination of Lipopolysaccharide and D(+)-Galactosamine-induced acute liver injury serves as an established animal model for fulminant hepatic failure[1].[2].
体内研究
D(+)-Galactosamine (700 mg/kg, i.p.) hydrochloride combined with Lipopolysaccharide(LPS, 10 μg/kg) creates an acute liver failure model in rats, displaying symptoms like anorexia, convulsion, syncope, and depression, with a mortality rate of 40.0% (36/90)[1].
D(+)-Galactosamine (400 mg/kg, i.p.) hydrochloride along with Lipopolysaccharide(LPS, 10 μg/kg) induces acute liver failure in C57BL/6J mice[2].
体外研究
D(+)-Galactosamine (5 mM, 0-24 h) hydrochloride triggers apoptosis and necrosis in rat hepatocyte primary cultures, activates caspase-3, and causes DNA fragmentation[3].
D-(+)-Galactosamine HCI/D-半乳糖胺盐酸盐 动物实验
Species
Animal Model
Administration
Dosage
Frequency
Description
References
Mice
LPS/D-GalN-induced acute liver injury model
Intraperitoneal injection
700 mg/kg
Single injection, sacrificed after 5 hours
To investigate the role of the Notch1-YAP pathway in acute liver injury. Results showed that Notch1-deficient mice exhibited reduced liver injury, decreased macrophage/neutrophil infiltration, lower pro-inflammatory cytokine expression, and increased anti-inflammatory cytokine expression.
Single dose, co-administered with endotoxin or TNF
D-galactosamine sensitizes mice to the lethal effects of endotoxin and TNF/cachectin by depleting uridine nucleotides, leading to liver injury.
J Exp Med. 1991 Feb 1;173(2):357-65
Wistar rats
Acute liver injury model
Intraperitoneal injection
400 mg/kg
Single injection, observed for 6 hours to 72 hours
D-GalN induced ALI via mitochondrial apoptosis- and proinflammatory cytokine-signaling pathways, leading to increased ROS production, hepatocyte apoptosis, and plasma multiple cytokines and chemokines. Green tea extract pretreatment attenuated these effects by enhancing anti-apoptotic mechanisms.
J Biomed Sci. 2009 Mar 25;16(1):35
Mice
GalN/LPS-induced acute liver failure model
Intraperitoneal injection
500 mg/kg
Single injection, observed for 24 hours
50-AMP pretreatment significantly increased survival rate, reduced serum AST and ALT levels, and attenuated liver necrosis and inflammatory cell infiltration
Cell Death Dis. 2014 Jan 9;5(1):e985
ICR mice
GalN/LPS-induced fulminant hepatic failure model
Intraperitoneal injection
800 mg/kg
Single injection, observed for 24 hours
To investigate the protective effect of afzelin against GalN/LPS-induced fulminant hepatic failure. Results showed that afzelin improved survival rate, reduced serum ALT levels and pro-inflammatory cytokines, and ameliorated mitochondrial function.
Br J Pharmacol. 2017 Jan;174(2):195-209
BALB/c mice
LPS/d-GalN-induced fulminant hepatic failure model
Intraperitoneal injection
600 mg/kg
Twice at a 12-h interval, followed by LPS/d-GalN challenge
To investigate the protective effect of AA against LPS/d-GalN-induced fulminant hepatic failure, it was found that AA pretreatment significantly increased survival rate, decreased ALT and AST levels, and alleviated liver pathological changes.
Front Immunol. 2017 Jul 7;8:785
C57BL/6 mice
Acute liver injury model induced by D-galactosamine/LPS (GalN/LPS)
Intraperitoneal injection
800 μg/g
Single injection, lasting 6 hours
Evaluate the effect of OCA on hepatocyte apoptosis in an acute liver injury model. OCA pretreatment did not significantly affect serum transaminase levels and hepatocyte apoptosis.
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