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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The turnover of 125I-labelled fibrinogen and 131I-labelled albumin was studied in the course of galactosamine-induced hepatitis in rabbits. In addition to galactosamine, some animals were treated with epsilon-aminocaproic acid (EACA) to inhibit the activation of the fibrinolytic system. The infusion of galactosamine and EACA caused generation of fibrin-rich microclots in the renal glomerular capillaries in seven out of 12 rabbits. Correspondingly, the incorporation of 125I-radioactivity into liver, spleen, and kidneys was pronounced in galactosamine- and EACA-treated rabbits compared with control animals treated with EACA. An acceleration of the 125I-fibrinogen elimination from the plasma was observed between eight and 12 hours after the start of the galactosamine infusion. The administration of heparin in addition to galactosamine and EACA prevented the occurrence of intravascular coagulation, but shortened the survival times of the animals because of bleeding into visceral organs. The elimination of 131I-albumin in plasma as well as the distribution of 131I-radioactivity in organs were similar in all the rabbits independent of the treatment with galactosamine, EACA, or heparin. The experiments indicate that, in addition to diminished synthesis of coagulation factors, disseminated intravascular coagulation is involved in galactosamine-induced hepatitis and contributes to the haemostatic disorder.
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PMID:Behaviour of 125I-fibrinogen and 131I-albumin in experimental galactosamine-induced hepatitis. 87 36

A novel compound N-(2-hydroxyethyl)-maleopimarimidyl morpholide (RU 18 492), was investigated for its effect against galactosamine induced hepatitis in rats. It was found to be active in reducing both serum transaminase levels and morphological changes due to the hepatotoxin. The protection was shown to be dose related and a significant reduction in liver damage was seen at doses of 50-400 mg/kg p.o. RU 18 492 was ineffective against carbon tetrachloride induced hepatitis in rats. It was suggested that the protective effect of RU 18 492 was due to its ability to stimulate the smooth endoplasmic reticulum thus inducing a more rapid detoxification of galactosamine.
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PMID:The protective effect of a novel compound RU 18492, on galactosamine-induced hepatotoxicity in the rat. 103 74

In adrenalectomized female rats a single dose of 375 mg D-galactosamine.HCl per kg of body weight produces both hepatitis and generalized edema with ascites. These alterations depend upon the dose and the time interval after injection of the aminosugar. The effect is specific for D-galactosamine; 2-deoxy-galactose produces only edema and no hepatitis, whereas D-glucosamine and D-galactose are without any measurable effect. In male adrenalectomized animals D-galactosamine produced hepatitis alone; fluid extravasation occurs only after additional orchiectomy. Glucocorticoids given before or simultaneously with D-galactosamine are able to prevent the animals from gettin edema and to ameliorate hepatitis, while mineralcorticoids do not show any effect on these alterations. It is evident that the effects of D-galactosamine on the hepatocyte and on the endothelial cells are independent from each other. This leads to the conclusion that D-galactosamine acts at least upon two different target organs, the liver and the reticulo-endothelial system in general.
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PMID:The appearance of D-galactosamine-induced hepatitis and generalized edema in adrenalectomized rats. 118 Aug 18

Four compounds, prednisolone, sodium phenobarbitone, azathioprine and orotic acid, were tested for their ability to inhibit galactosamine induced hepatitis in the rat. Prednisolone offered total protection at doses of 100 mg/kg and above; sodium phenobarbitone and orotic acid modified the response to galactosamine and azathioprine was without effect.
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PMID:Inhibition, by drugs, of galactosamine induced hepatitis in the rat. 124 44

An experimental hepatitis was induced in rabbits by intravenous infusion of 1 g galactosamine per kilogram of body weight. Galactosamine administration caused microclot formation in kidneys, liver, lungs, and spleen in a low percentage. If, however, animals were infused with the fibrinolysis inhibitor epsilon-aminocaproic acid in addition to galactosamine, microclots were generated in a high percentage. The microclots exhibited typical staining characteristics like those observed in the generalized Shwartzman reaction. Some animals developed bilateral renal cortical necrosis. Heparin treatment prevented the occurrence of microclot fromation after galactosamine administration, but it neither prolonged the survival time of the animals nor prevented or reduced liver cell damage. Increases in serum GPT and bilirubin levels were similar in heparin-treated and untreated rabbits. The experiments indicate that disseminated intravascular coagulation is involved in galactosamine-induced hepatitis but does not contribute to the severity of the liver injury.
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PMID:Experimental galactosamine-induced hepatitis. Effect of anticoagulant and antifibrinolytic agents on microclot formation. 125 92

Oral pretreatment with E3330, a novel quinone derivative, attenuated liver injury induced with tumor necrosis factor-alpha in galactosamine-sensitized mice. Tumor necrosis factor-alpha is known to induce inflammatory mediators such as leukotrienes and prostanoids. An in vitro study showed that E3330 inhibited the generation of leukotriene B4 and thromboxane B2, but enhanced prostaglandin E2 generation from rat peritoneal exudate cells stimulated with the Ca(2+)-ionophore, A23187. These findings suggest that the protective effect of E3330 on galactosamine/tumor necrosis factor-alpha hepatitis is due at least in part to its inhibition of the generation of leukotrienes. The inhibition of thromboxane B2 generation or the enhancement of prostaglandin E2 generation by E3330 may also contribute to its hepatoprotective effect.
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PMID:Protective effects of E3330, a novel quinone derivative, on galactosamine/tumor necrosis factor-alpha-induced hepatitis in mice. 133 20

Pretreatment with recombinant human granulocyte CSF (G-CSF) protected mice in two different models of septic shock. Intravenous injection of 250 micrograms/kg G-CSF to mice prevented lethality induced by 5 mg/kg LPS. Injection of 50 micrograms/kg G-CSF protected galactosamine-sensitized mice against LPS-induced hepatitis. In either case, this protection was accompanied by a suppression of LPS-induced serum TNF activity. 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. The suppressive effect of G-CSF on LPS-induced TNF production was also demonstrated in rats. In vivo, no TNF was detectable in the blood of LPS-treated rats, which had been pretreated with G-CSF. Ex vivo, alveolar macrophages, bone marrow macrophages, Kupffer cells, or peritoneal macrophages prepared from G-CSF-treated rats produced significantly less TNF upon stimulation with LPS than corresponding populations from control rats. However, when these macrophage populations were incubated with G-CSF in vitro, LPS-induced TNF production was unaffected. These data suggest that the G-CSF-mediated suppression of TNF production is not a direct effect of G-CSF on macrophages. To examine whether, independent of the protection against LPS, G-CSF treatment still activated neutrophils, it was demonstrated that granulocytes from G-CSF-treated rats were primed for PMA-induced oxidative burst and for ionophore/arachidonic acid-stimulated lipoxygenase product formation. The experiments of this study support the notion that G-CSF is a negative feedback signal for macrophage-derived TNF-alpha production during Gram-negative sepsis.
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PMID:Granulocyte colony-stimulating factor treatment protects rodents against lipopolysaccharide-induced toxicity via suppression of systemic tumor necrosis factor-alpha. 137 68

Administrations of hepatotoxicants namely carbon tetrachloride (CCl4:0.4 ml in 1.2 ml of liquid paraffin) and ANIT (1 ml of 1.5% solution in liquid paraffin) in Charles foster rats (force fed) and D-galactosamine (8 mg in water per swiss albino mouse, ip) induce the release of TNF-alpha in case of CCl4 and D-galactosamine. High TNF-alpha level was observed up to 48 hr in CCl4 and up to 24 hr in D-galactosamine treated animals. Elevated levels of biochemical like ALP and SGPT are also recorded. TNF-alpha level can be measured of tissue damage and prognosis in case of hepatitis.
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PMID:Induction of tumour necrosis factor alpha in experimental animals treated with hepatotoxicants. 145 48

The present study examined the preventive effects of green tea extract on D-galactosamine (GalN)-induced hepatic injury in rats, an animal model of viral hepatitis. A single i.p.-injection of GalN (700 mg/kg) to male Wistar rats caused fulminant hepatitis by 48 hr as assessed by marked increases in the serum aspartate aminotransferase (GOT), alanine aminotransferase (GPT) and alkaline phosphatase (ALP) activities; decreases in the serum protein and cholesterol levels and the amount of liver microsome P-450; and marked changes in organ weights. The lecithin: cholesterol acyltransferase (LCAT) activity markedly increased at 8 hr and markedly decreased at 24 hr after the GalN injection. In the experiment, animals were orally administered green tea extract at doses of 50, 100 or 200 mg/kg five times each before and after the GalN injection. Treatment with green tea extract significantly prevented the increases in the GOT, GPT and ALP activities in a dose-related manner. It also significantly prevented the decreases in serum albumin and total cholesterol, although not in a dose-related manner. A tendency to prevent the increase in LCAT activity and the decrease in liver microsome P-450 was also noted. Little effect was found on the other abnormal changes in the serum lipids and proteins and the organ weights. These results suggest that green tea may have an ameliorating effect on hepatic dysfunction.
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PMID:[Effects of green tea extract on galactosamine-induced hepatic injury in rats]. 146 98

1. 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. Since LPS and these cytokines induce ornithine decarboxylase (ODC) and histidine decarboxylase (HDC) in the liver and spleen of mice, the effects of GalN on the induction of ODC and HDC in these organs were examined. 2. The induction of ODC by LPS, IL-1 or TNF was suppressed by GalN in the liver, and this suppression preceded the hepatic congestion. There was good agreement between the degree of hepatic congestion and the suppression of ODC induction by various amounts of GalN. The induction of ODC in the spleen was suppressed only at the highest dose of GalN examined. 3. GalN is known to deplete uridine 5'-triphosphate (UTP), resulting in the suppression of RNA and protein synthesis. An injection of uridine, the precursor of UTP, diminished the GalN-induced suppression of ODC induction by LPS and prevented the hepatic congestion and death. 4. LPS-pretreatment before injection of LPS plus GalN prevented the suppression of ODC activity and prevented the hepatic congestion and death. 5. An injection of putrescine, the product of ODC, prolonged survival time and delayed the development of hepatic congestion. However, injection of an ODC inhibitor into the mice given LPS did not produce hepatic congestion. 6. The induction of HDC in the liver by LPS, IL-1 or TNF was not suppressed by GalN and, at high doses, the response to LPS was enhanced. An inhibitor of HDC neither prevented the hepatic congestion nor enhanced the protective effect of putrescine.7. Although GalN in combination with IL-la induced a markedly higher HDC activity than was observed when it was combined with TNFa, and suppressed the induction of ODC, the former combination at the doses used did not produce hepatic congestion or death. However, the sensitization to TNFa by GalN was markedly potentiated by IL-la.8. 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. These results are consistent with the hypothesis that both IL-1 and TNF are involved in the sensitization to LPS.
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PMID:Ornithine and histidine decarboxylase activities in mice sensitized to endotoxin, interleukin-1 or tumour necrosis factor by D-galactosamine. 147 81


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