On the mechanism of action of galactosamine: Different response tod-galactosamine of rat liver during development

Reutter, Werner; Bauer, Ch.; Lesch, R

doi:10.1007/bf00598804

Cited by 29 publications

(7 citation statements)

References 3 publications

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“…It should be noted in this study that D -GalN sensitization varies with age. 34 Previous study showed that the basal level of Stat3 in liver does not significantly change at various ages of mice, but the activation of Stat3 is impaired in aged animals. 35 Therefore, the study needs to be conducted in mice with the same or similar age to avoid the impact of age.…”

Section: Discussionmentioning

confidence: 96%

Stattic alleviates acute hepatic damage induced by LPS/d-galactosamine in mice

et al. 2021

Innate Immun

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Increasing evidence indicates that signal transducer and activator of transcription 3 (STAT3), a vital transcription factor, plays crucial roles in the regulation of inflammation. STAT3 has become a novel therapeutic target for intervention in inflammation-related disorders. However, it remains unclear whether STAT3 plays a part in acute hepatic damage. To investigate the effects of STAT3 here, LPS/d-GalN-induced hepatic damage was induced in mice, the STAT3 inhibitor Stattic was administered, and the degree of liver injury, inflammation, and hepatocyte apoptosis were investigated. The results showed that Stattic mitigated the hepatic morphologic abnormalities and decreased the level of aminotransferase in LPS/D-GalN-insulted mice. The results also indicated that Stattic decreased the levels of TNF-α and IL-6, prevented the activation of the caspase cascade, suppressed cleavage of PARP, and decreased the quantity of TUNEL-positive cells. These results suggest that Stattic provided protective benefits in LPS/d-GalN-induced hepatic damage, and the protective effects might be associated with its anti-inflammatory and anti-apoptotic effects. Therefore, STAT3 might become a novel target for intervening in inflammation-based and apoptosis-based hepatic disorders.

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Section: Discussionmentioning

confidence: 96%

Stattic alleviates acute hepatic damage induced by LPS/d-galactosamine in mice

et al. 2021

Innate Immun

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“…In addition to LPS, hepatic inflammation may also be induced by injection of D-galactosamine (GAIN). This prototype liver-specific toxin acts by sensitizing the liver towards the effects of endogenous or exogenously applied LPS (Galanos et al 1979;review in Leist et al 1995a) and has been shown to induce hepatocyte destruction and apoptosis (Reutter et al 1968(Reutter et al , 1970Keppler et al 1968). …”

Section: Inflammation and Hepatic Apoptosismentioning

confidence: 99%

“…Selective liver failure caused by this substance in rodents was suggested 30 years ago to represent a model for human viral hepatitis (Keppler et al 1968). In fact, hepatocyte apoptosis (Councilman bodies) was noted to be one of the most conspicuous phenomena of GaiN-induced pathology (Reutter et al 1968(Reutter et al , 1970Keppler et al 1968;Medline et al 1970). A series of studies in the 1970s and 1980s showed that the substance exerted a very pronounced toxicity in synergy with endogenous and exogenous immune modulators (Grtin and Liehr 1976;Liehr et al 1978;Mihas et al 1990;Galanos et al 1979;Czaia et al 1994).…”

Section: Tnf As Mediator Of Toxin-induced Apoptosismentioning

confidence: 99%

Cytokine-mediated hepatic apoptosis

Leist

Gantner

Künstle

et al. 1998

Reviews of Physiology Biochemistry and Pharmacology, Volume 133

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“…They are as follows: the stimulation of hepatic regeneration, which makes the liver resistant to damage by hepatotoxins (8) and activation of the functions of the reticuloendothelial system (9) or the biosynthesis of protein (10).…”

mentioning

confidence: 99%

The protective effects of (4R)-hexahydro-7,7-dimethyl-6-oxo-1,2,5-dithiazocine-4-carboxylic acid (SA3443), a novel cyclic disulfide, on chemically-induced acute liver injury.

et al. 1991

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ABSTRACT-The effects of SA3443, a novel cyclic disulfide compound, on acute liver injuries induced by carbon tetrachloride (CC14), D-galactosamine and DLethionine were studied in rats or mice. SA3443 (100-300 mg/kg, p.o.) significantly suppressed the increases of serum transaminase activity and liver triglyceride content in the CC14 or DL-ethionine-induced model. Furthermore, SA3443 (300 mg/kg, p.o.) clearly reduced the formation of hepatic lipid peroxide in CCl4-treated rats. These results indicate that SA3443 protects the liver against acute liver injury.It is well-known that the administration of carbon tetrachloride (CC14), ethionine and galactosamine lead to various forms of liver damage (1, 2). These chemically-induced liver injuries include membrane fragility, enzyme leakage and pathological degeneration of the hepatotoxic mechanism (2). These chemicallyinduced liver injury models have therefore been utilized to screen and investigate many hepatoprotective agents.(4R)-Hexahydro-7,7-dimethyl-6-oxo-1,2,5-dithiazocine-4-carboxylic acid (SA3443) is a novel cyclic disulfide compound that was developed as an anti-hepatitis agent. In pharmacological studies, SA3443 was found to be effective in preventing immunologically-induced liver injuries in models (3). These findings suggest that SA3443 would be useful as a protective agent in the treatment of liver diseases. The purpose of the present study was to clarify the hepatoprotective effects of SA3443, using three classical models, CC14-, ethionineand galactosamine-induced acute liver injuries in rats or mice.Male Wistar rats weighing 200 -240 g were used for the CC14 and D-galactosamine-induced liver injury model, and male BALB/c mice weighing 20-25g were used for the ethionine model. To induce liver injuries using CC14 and galactosamine, the animals were fasted for 18 hr before intoxication. CC14 (5 ml/kg) in the form of a 5% (v/v) solution in olive oil was given to rats by intraperitoneal (i.p.) injection. D-Galactosamine (400 mg/kg) was given by i.p. injection. SA3443 suspended in a 1.0% (w/v) methylcellulose solution was administered p.o. at doses of 100 and 300 mg/kg 30 min before CC14 or galactosamine intoxication. The animals were killed 24 hr after the injection of CC14 or galactosamine, and blood samples were taken. The transaminase activities were then measured according to the method used by Karmen (4). The liver weight was measured at the time of killing. DL-

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On the mechanism of action of galactosamine: Different response tod-galactosamine of rat liver during development

Cited by 29 publications

References 3 publications

Stattic alleviates acute hepatic damage induced by LPS/d-galactosamine in mice

Stattic alleviates acute hepatic damage induced by LPS/d-galactosamine in mice

Cytokine-mediated hepatic apoptosis

The protective effects of (4R)-hexahydro-7,7-dimethyl-6-oxo-1,2,5-dithiazocine-4-carboxylic acid (SA3443), a novel cyclic disulfide, on chemically-induced acute liver injury.

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