Macrophages from rat livers with micronodular and macronodular cirrhosis differ with respect to mediator release and DNA-synthesis

Vogl, S.; Junker, U.; Vogelsang, Heinz; Dargel, R.

doi:10.1016/s0168-8278(97)80118-3

Cited by 9 publications

(8 citation statements)

References 38 publications

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“…Earlier studies have demonstrated functional differences in liver macrophages isolated from micro or macronodular cirrhosis. Macrophages from rat livers with micronodular and macronodular cirrhosis differ with respect to mediator release and DNA‐synthesis 43 …”

Section: Discussionmentioning

confidence: 99%

Oxidative stress in the development of liver cirrhosis: A comparison of two different experimental models

Natarajan

Thomas

Ramamoorthy

et al. 2006

J of Gastro and Hepatol

107

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Section: Discussionmentioning

confidence: 99%

Oxidative stress in the development of liver cirrhosis: A comparison of two different experimental models

Natarajan

Thomas

Ramamoorthy

et al. 2006

J of Gastro and Hepatol

107

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“…23,28 Part of the mechanism of action of cytokine induced hepatotoxicity is explained by the oxidant stress that is involved. In a study by Sanz et al TAA in necrogenic dose was shown to increase MDA, SOD, GSH-Px, catalase and glutathione-S-reductase levels and decrease GSH level in hepatocyte cultures.…”

Section: Discussionmentioning

confidence: 99%

Serum cytotoxin and oxidant stress markers in N-acetylcysteine treated thioacetamide hepatotoxicity of rats

Akbay

Çınar²,

Uzunalımoǧlu

et al. 1999

Hum Exp Toxicol

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N-acetylcysteine (NAC) is a glutathione precursor used to treat several clinical conditions where intracellular oxidant-antioxidant balance is disturbed, among which, acetaminophen induced hepatotoxicity may be counted. In this study, administering thioacetamide (TAA) as a hepatotoxic agent, a rat model of hepatotoxicity has been established, to investigate some of the immune mediated basic oxidant-antioxidant homeostatic mechanisms involved, and potential serum markers for follow-up of disease and treatment. To do this, four experimental groups receiving saline/saline, saline/NAC, saline/TAA and NAC/TAA as intraperitoneal injections, have been formed. Rat serum tumor necrosis factor-a (TNF-α), Interleukin1-β (IL1-β), malondialdehyde (MDA) as a measure of final oxidant damage and the antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) have been assayed. Hepatocellular damage has been measured via the biochemical estimates ALT, AST and LDH as well as histopathological grading. It was found that both TNF-α and IL1-β were significantly elevated in saline/TAA receivers (P50.01) when compared to NAC/TAA receivers. Serum MDA was also increased in TAA receivers in addition to SOD (P50.05) and GSH-Px (P50.05). Serum nitrite levels have also been assayed to give an estimate of nitric oxide that is suggested as a counter-balancer of oxidant stress. NAC/saline receivers had the highest levels of nitrites in the serum (P50.05). Our results indicate that part of the hepatocellular injury to rat liver, induced by TAA is mediated by oxidative stress caused by the action of cytokines imparted by the enzymatic SOD and GSH-Px and non-enzymatic gaseous nitric oxide mechanisms causing an alleviation on administration of NAC. In addition, TNF-α,IL1-β,MDA, SOD, GSH-Px and nitrites are potential candidates of serum indicators for monitorization of pathophysiological stage of liver disease.

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“…KC and SEC from normal and cirrhotic rat livers were isolated by liver enzymatic perfusion, gradual digestion, density gradient centrifugation and counterflow elutriation as described previously [43] with slight modifications [40,44]. In brief, livers were perfused with 0.45% (control livers) or 0.55% (cirrhotic livers) pronase E and with 0.03% (controls) or 0.04% (cirrhotic livers) collagenase, respectively, for 20 min.…”

Section: Isolation Of Rat Nonparenchymal Liver Cellsmentioning

confidence: 99%

“…Fractions enriched with SEC and KC were collected at flow rates of 27.5 and 47.5 mL/min, respectively. The purity of isolated nonparenchymal liver cells was evaluated as described earlier [11,40,44]. Nonparenchymal liver cells were evaluated by immunofluorescence for the presence of fibulin-2 (marker for liver myofibroblasts), desmin (marker for hepatic stellate cells), von Willebrand factor (marker for SEC), ED2 (marker for KC) and albumin (marker for hepatocytes).…”

Section: Isolation Of Rat Nonparenchymal Liver Cellsmentioning

confidence: 99%

Expression of insulin-like growth factor-I and insulin-like growth factor binding proteins during thioacetamide-induced liver cirrhosis in rats

Novosyadlyy

Dargel

Scharf

2005

Growth Hormone & IGF Research

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Macrophages from rat livers with micronodular and macronodular cirrhosis differ with respect to mediator release and DNA-synthesis

Cited by 9 publications

References 38 publications

Oxidative stress in the development of liver cirrhosis: A comparison of two different experimental models

Oxidative stress in the development of liver cirrhosis: A comparison of two different experimental models

Serum cytotoxin and oxidant stress markers in N-acetylcysteine treated thioacetamide hepatotoxicity of rats

Expression of insulin-like growth factor-I and insulin-like growth factor binding proteins during thioacetamide-induced liver cirrhosis in rats

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