Increased Oxidative Stress in Dimethylnitrosamine-Induced Liver Fibrosis in the Rat: Effect of N-Acetylcysteine and Interferon-α

Vendemiale, Gianluigi; Grattagliano, Ignazio; Caruso, Maria Lucia; Serviddio, Gaetano; Valentini, Anna Maria; Pirrelli, M; Altomare, Emanuele

doi:10.1006/taap.2001.9234

Cited by 99 publications

(72 citation statements)

References 54 publications

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“…Through this hepatic fibrosis model, the effects of melatonin on hepatic fibrosis induced by CCl 4 in rats were examined. N-acetylcysteine (NAC), a free radical scavenger, is a glutathione precursor which increases glutathione levels in hepatocytes [15,16] . Increased glutathione levels limit the production of reactive oxygen species (ROS) which can cause hepatocellular injury.…”

Section: Discussionmentioning

confidence: 99%

Melatonin ameliorates experimental hepatic fibrosis induced by carbon tetrachloride in rats

Ren¹,

Xu²,

Qiao³

2009

WJG

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AIM:To investigate the protective effects of melatonin on carbon tetrachloride (CCl 4 )-induced hepatic fibrosis in experimental rats. METHODS:All rats were randomly divided into normal control group, model control group treated with CCl 4 for 12 wk, CCl 4 + NAC group treated with CCl 4 + NAC (100 mg/kg, i.p.) for 12 wk, CCl 4 + MEL-1 group treated with CCl 4 + melatonin (2.5 mg/kg) for 12 wk, CCl 4 + MEL-2 group treated with CCl 4 + melatonin (5.0 mg/kg) for 12 wk, and CCl 4 + MEL-3 group treated with CCl 4 + melatonin (10 mg/kg). Rats in the treatment groups were injected subcutaneously with sterile CCl 4 (3 mL/kg, body weight) in a ratio of 2:3 with olive oil twice a week. Rats in normal control group received hypodermic injection of olive oil at the same dose and frequency as those in treatment groups. At the end of experiment, rats in each group were anesthetized and sacrificed. Hematoxylin and eosin (HE) staining and Van Gieson staining were used to examine changes in liver pathology. Serum activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and protein concentration were measured with routine laboratory methods using an autoanalyzer. Hydroxyproline (HYP) content in liver and malondialdehyde (MDA) and glutathione peroxidase (GPx) levels in liver homogenates were assayed by spectrophotometry. Serum hyaluronic acid (HA), laminin (LN), and procollagen Ⅲ N-terminal peptide (PⅢNP) were determined by radioimmunoassay. RESULTS:Pathologic grading showed that the fibrogenesis was much less severe in CCl 4 + MEL3 group than in model control group (u = 2.172, Moreover, treatment with melatonin (5, 10 mg/kg) significantly reduced the MDA content and increased the GPx activity in liver homogenates compared with model control group (MDA: 7.89 ± 1.49 noml/mg prot vs 6.29 ± 1.42 noml/mg prot and 6.25 ± 2.27 noml/mg prot, respectively, P = 0.015, P = 0.015; GPx: 49.13 ± 8.72 U/mg prot vs 57.38 ± 7.65 U/mg prot and 61.39 ± 13.15 U/mg prot, respectively, P = 0.035, P = 0.003). CONCLUSION:Melatonin can ameliorate CCl 4 -induced hepatic fibrosis in rats. The protective effect of melatonin on hepatic fibrosis may be related to its antioxidant activities.

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Section: Discussionmentioning

confidence: 99%

Melatonin ameliorates experimental hepatic fibrosis induced by carbon tetrachloride in rats

Ren¹,

Xu²,

Qiao³

2009

WJG

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“…Animal care and all experimental procedures were conducted in accordance with the guide for animal experiments edited by the Korea Academy of Medical Science. The animals were housed in an air-conditioned room at 25 C with a 12-h dark/light cycle. All animals received humane care during the study, and unlimited access to food and water.…”

Section: Methodsmentioning

confidence: 99%

Suppression by Fucoidan of Liver Fibrogenesisviathe TGF-β/Smad Pathway in Protecting against Oxidative Stress

Hong

Jung

Lee

et al. 2011

Bioscience, Biotechnology, and Biochemistry

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“…Most have shown conclusive effects in various in vitro and experimental models of liver fibrogenesis (CCl 4 -induced fibrosis or bile duct-ligated models) [110,111].…”

Section: Inhibition Of Hsc Activationmentioning

confidence: 99%

Liver extracellular matrix in health and disease

Bédossa

Paradis

2003

The Journal of Pathology

246

213

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Liver fibrosis is the hallmark of every chronic liver disease. It is also the major factor of morbidity and mortality due to the development of cirrhosis and its complications including hepatocellular carcinoma. But even at the beginning of the process of liver fibrosis and due to the strategic position of the extracellular matrix at the interface between blood flow and epithelial compartment, any quantitative or qualitative modification of extracellular matrix will rapidly affect structure and function of the liver. The development of several animal models of liver fibrosis as well as isolation and cultivation of hepatic stellate cells, the major fibrogenic cell type in the liver, led to the gathering of recent knowledge on the mechanism of liver fibrosis. Activation of hepatic stellate cells is a key event in this process and many details on this finely tuned mechanism are now available. In addition to these experimental data, experience from chronic hepatitis C now allows the development of new concepts and perspectives such as liver fibrosis regression and antifibrotic therapies.

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Increased Oxidative Stress in Dimethylnitrosamine-Induced Liver Fibrosis in the Rat: Effect of N-Acetylcysteine and Interferon-α

Cited by 99 publications

References 54 publications

Melatonin ameliorates experimental hepatic fibrosis induced by carbon tetrachloride in rats

Melatonin ameliorates experimental hepatic fibrosis induced by carbon tetrachloride in rats

Suppression by Fucoidan of Liver Fibrogenesisviathe TGF-β/Smad Pathway in Protecting against Oxidative Stress

Liver extracellular matrix in health and disease

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