Monitoring of serum markers for fibrosis during CCl 4 -induced liver damage

Jiang, Zhaoyan; You, Da yu; Chen, Xiang chi; Wu, Jian

doi:10.1016/s0168-8278(05)80658-0

Cited by 33 publications

(15 citation statements)

References 33 publications

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“…In our study, we substantiated the impression that pathological changes taking place in CCl 4 -induced model were different from those in DMN-induced model [22,26] . But, all the animals in fibrotic model groups showed complete fibrotic septum, forming a pattern of micronodular cirrhosis.…”

Section: Discussionsupporting

confidence: 81%

“…CCl 4 is one of the most widely used hepatic toxins for experimental induction of liver fibrosis cirrhosis in laboratory [22,25,26] . The model was used even in 1936.…”

Section: Discussionmentioning

confidence: 99%

“…In the former, besides hepatocyte necrosis, fatty degeneration was the major feature [22] while in the latter, lymphomonocyte infiltration and local hepatocyte necrosis were the main characteristics [23] . However, after 12 weeks of CCl 4 and 8 weeks of DMN treatment, all the rats in fibrotic model groups showed complete fibrotic septum, forming a pattern of micronodular cirrhosis to the parenchyma (Figure 1).…”

Section: Animal Experimentsmentioning

confidence: 99%

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Animal experiment and clinical study of effect of gamma-interferon on hepatic fibrosis

Weng

Cai²,

Liu³

2001

WJG

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Section: Discussionsupporting

confidence: 81%

“…CCl 4 is one of the most widely used hepatic toxins for experimental induction of liver fibrosis cirrhosis in laboratory [22,25,26] . The model was used even in 1936.…”

Section: Discussionmentioning

confidence: 99%

Section: Animal Experimentsmentioning

confidence: 99%

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Animal experiment and clinical study of effect of gamma-interferon on hepatic fibrosis

Weng

Cai²,

Liu³

2001

WJG

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“…Carbon tetrachloride is given to rodents typically through either subcutaneous injection or gavage of 1–2 ml/kg of 50% CCl 4 twice weekly [45]. In this model, significant hepatocyte necrosis, inflammatory infiltration, proliferation of hepatic stellate cells, and connective tissue deposition are prominent features observed in the liver of rats after 6–9 weeks of CCl 4 treatment [45]. DMNS and TAA are hepatic carcinogens that effectively induce severe liver fibrosis and cirrhosis in rodents in as little as 1–2 months of treatment [46,47].…”

Section: Alternative Models Of Experimental Alcoholic Liver Diseasementioning

confidence: 99%

Animal Models of Alcoholic Liver Disease

Arteel¹

2010

Dig Dis

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The risk of alcohol-induced liver disease (ALD) increases dose- and time-dependently with consumption of alcohol. The progression of the disease is well characterized; however, although the progression of alcohol-induced liver injury is well characterized, there is no universally-accepted therapy available to halt or reverse this process in humans. With better understanding of the mechanism(s) and risk factors that mediate the initiation and progression of this disease, rational targeted therapy can be developed to treat or prevent it in the clinics. Several models for experimental ALD exist, including non-human primates, micropigs and rodents. However, most researchers employ rodent models of ALD. Furthermore, the advent of genetically modified strains of rodents (e.g. ‘knockout’ mice) has increased the specificity of the hypotheses that can be directly tested. Based on these models systems, several plausible hypotheses to explain the mechanism(s) by which alcohol leads to liver damage have been proposed, including consequences of alcohol metabolism, oxidative/nitrosative stress, altered inflammatory responses, and increased sensitivity to cytotoxic stimuli. These studies have also identified candidate genes for polymorphism studies to explain potential increased genetic risk in some individuals. However, despite significant advances in our understanding of the mechanisms by which ALD develops based on studies with these models, this work has yet to translate to a viable therapy for ALD in the clinics. This talk will also discuss potential reasons for these limitations to date and suggest future prospects to improve the translational utility of modeling ALD.

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“…Besides, as in the first experiment colchicine at a dose of 1 mg/kg resulted in 60% mortality, in the second experiment colchicine was given at a lower dosage (100 lg/kg) and not daily but at repeated doses of once a week. Colchicine at a dose of 50 lg/kg a day has been shown to reduce hepatic fibrosis in rats with bile duct ligation, and carbon tetrachloride-in- [17,18]. Besides, administration of colchicine at a dose of 30 lg/kg a day resulted in the development of significantly less interstitial fibrosis due to chronic cyclosporine toxicity in rats [3].…”

Section: Discussionmentioning

confidence: 99%