Is Cirrhosis of the Liver Experimentally Produced by CC14 an Adequate Model of Human Cirrhosis?

Tamayo, Ruy Pérez

doi:10.1002/hep.1840030118

Cited by 277 publications

(76 citation statements)

References 70 publications

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“…When we evaluated lipid peroxidation in the two models of cirrhosis, animals in the EX group had significantly higher values compared to those in the CO group, and the level of TBARS and QL were elevated in the lung and liver in both groups. This overproduction of ROS might occur in several pathophysiological situations and may explain the finding that in our study, the levels of TBARS and QL were high (22,23) . Physiological defense mechanisms are effective in preventing or counteracting the damage caused by free radicals, which can include a set of endogenous antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx).…”

Section: Discussionsupporting

confidence: 54%

“…The CCl 4 trichloromethyl radical is converted to (•CCL 3 ) and trichloromethyl peroxide (°OOCCl 3 ). The CCl 4 trichloromethyl radical has been described as causing hepatotoxic effects such as fibrosis, steatosis, necrosis and hepatocellular carcinoma (9,22) . Bile duct ligation is another experimental model related to secondary biliary cirrhosis because it causes cell proliferation, hepatocellular necrosis, apoptosis, activation of stellate cells, and finally the formation of liver fibrosis and cirrhosis.…”

Section: Lung and Liver Changes Due To The Induction Of Cirrhosis In mentioning

confidence: 99%

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Lung and Liver Changes Due to the Induction of Cirrhosis in Two Experimental Models

Ferrari

Tieppo

Rosa

et al. 2013

Arq. Gastroenterol.

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-Context -To evaluate lung and liver changes in two experimental models using intraperitoneal carbon tetrachloride (CCl 4 ) and bile duct ligation (BDL). Methods -Twenty-four male Wistar rats were divided into a control group (CO) and an experimental group (EX). We evaluated the liver transaminases (AST, ALT, AP), arterial blood gases (PaO 2 , PCO 2 and SpO 2 ) and lipid peroxidation by TBARS (substances that react to thiobarbituric acid) and chemiluminescence. We also evaluated the antioxidant enzyme superoxide dismutase (SOD) and histology of lung tissue and liver. Results -There were significant differences in AST, ALT, ALP and PaO 2 between CO group and EX group (P<0.05). The levels of TBARS, chemiluminescence and activity of enzyme superoxide dismutase were increased to different degrees in the CCl 4 groups: CO and in the BDL -EX (P<0.05, respectively). In the lung histology, an increase in the wall thickness of the pulmonary artery and a diameter reduction in the CCl 4 animal model were observed: comparing CO group with EX group, we observed a reduction in thickness and an increase in the diameter of the artery wall lung. Conclusion -Both experimental models have caused liver damage and alterations in the artery wall that are associated with major changes in pulmonary gas exchange.

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Section: Discussionsupporting

confidence: 54%

Section: Lung and Liver Changes Due To The Induction Of Cirrhosis In mentioning

confidence: 99%

Lung and Liver Changes Due to the Induction of Cirrhosis in Two Experimental Models

Ferrari

Tieppo

Rosa

et al. 2013

Arq. Gastroenterol.

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“…Leukamenin F attenuated CCl 4 -induced liver fibrosis in mice As reported, prolonged low dose CCl 4 administration induces hepatic fibrogenesis, which largely resembles the hepatic fibrosis in human disease [22] . We thereby constructed the CCl 4 -induced mouse hepatic fibrosis model for the current research.…”

Section: Resultssupporting

confidence: 54%

Leukamenin F suppresses liver fibrogenesis by inhibiting both hepatic stellate cell proliferation and extracellular matrix production

et al. 2010

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Aim: To investigate the inhibitory effect of the natural product Leukamenin F on liver fibrosis and explore its potential underlying mechanisms. Methods: Carbon tetrachloride (CCl 4 )-treated mouse model in vivo and in hepatic stellate cells (HSC) in vitro were used. The effect on CCl 4 -induced liver fibrosis was studied using histochemical and biochemical analysis, while the inhibition on HSC was assessed using cell proliferation/apoptosis assay and collagen I production using real-time PCR. The inhibitory effects of Leukamenin F on Akt/mTOR/ p70S6K and TGFβ/Smad pathways was studied using Western blot and cell image analysis. Results: Leukamenin F (0.1-1 mg/kg, ip, q.d.×28) significantly reduced α-SMA and collagen specific Sirius red staining areas in CCl 4 -treated mouse livers. This compound at 1-2 µmol/L dose-dependently inhibited α-SMA expression, cell proliferation and type I procollagen mRNA expression in activated HSC. Furthermore it inhibited the Akt/mTOR/p70S6K pathway and suppressed TGFβ -induced Smad2/Smad3 phosphorylation and nuclear translocation in HSC. Conclusion: Our results demonstrated that Leukamenin F could attenuate CCl 4 -induced liver fibrogenesis in mice as an efficient inhibitor against both HSC proliferation and ECM production. This natural product provides a valuable structural hint for the development of anti-liver fibrosis reagents.

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“…CCl 4 -induced liver injury, which shows many similarities with human liver injury, is a common model for studying the mechanisms of liver injury and the therapeutic effects of drugs (Fort et al 1998;Tamayo 2007). In this study, CCl 4 -induced chronic liver injury was established to examine the effects of ICA-treated hUMSCs administration in the chronic liver injury model.…”

Section: Discussionmentioning

confidence: 99%

Icariin-treated human umbilical cord mesenchymal stem cells decrease chronic liver injury in mice

et al. 2016

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Human umbilical cord mesenchymal stem cells (hUMSCs) have been shown to have multiple differentiation potentials. However, a key problem is that only a small number of hUMSCs can migrate to damaged tissue after transplantation. According to ''The Theory of Kidney Essence'' in Traditional Chinese Medicine, some traditional Chinese medicines used for tonifying the kidneys can be applied in promoting the differentiation and migration of stem cells in vivo. Our previous study demonstrated that icariin (ICA) could up-regulate the pluripotent genes of hUMSCs in vitro and induce cell migration in mice in an acute kidney injury model in vivo. The aim of this study was to investigate the effects of ICAinduced hUMSCs in chronic liver injury (CLI) caused by carbon tetrachloride (CCl 4 ). CLI was induced by intraperitoneal injection of CCl 4 . ICA-treated hUMSCs were transplanted via intra-venous injection. The animals were followed for survival, biochemistry analysis and pathology. The results show that ICAtreated hUMSCs accelerate the recovery of liver function in mice with CLI. In addition, ICA-treated hUMSCs increase the anti-oxidant activities in liver and prevent the progression to hepatic fibrosis. Moreover, ICA induces the migration of hUMSCs to the injured liver tissue. In conclusion, these data demonstrate that ICA-treated hUMSCs exhibit recovery and protective properties in the mice model of CCl 4 -induced CLI.

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Is Cirrhosis of the Liver Experimentally Produced by CC14 an Adequate Model of Human Cirrhosis?

Cited by 277 publications

References 70 publications

Lung and Liver Changes Due to the Induction of Cirrhosis in Two Experimental Models

Lung and Liver Changes Due to the Induction of Cirrhosis in Two Experimental Models

Leukamenin F suppresses liver fibrogenesis by inhibiting both hepatic stellate cell proliferation and extracellular matrix production

Icariin-treated human umbilical cord mesenchymal stem cells decrease chronic liver injury in mice

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