Taurine inhibits oxidative damage and prevents fibrosis in carbon tetrachloride-induced hepatic fibrosis

Miyazaki, Teruo; Karube, Masaaki; Matsuzaki, Yasushi; Ikegami, Tadashi; Doy, Mikio; Tanaka, Naomi; Bouscarel, Bernard

doi:10.1016/j.jhep.2005.01.033

Cited by 95 publications

(58 citation statements)

References 49 publications

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“…CCl 4 induces fibrosis liver cirrhosis and may be used for the study of PPH. The signals observed in the CCl 4 liver injury model are similar to those found in cirrotic patients (19) . The CCl 4 trichloromethyl radical is converted to (•CCL 3 ) and trichloromethyl peroxide (°OOCCl 3 ).…”

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

confidence: 74%

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

confidence: 74%

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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“…6,7,30 Treatment with the antioxidant taurine was shown to attenuate hepatic fibrosis by inhibiting oxidative stress and TGF-b gene expression. 31 In this study, kallistatin decreased the levels of the profibrotic molecules such as TGF-b1 and PAI-1 in the ischemic myocardium, and directly inhibited TGF-b1-induced collagen I synthesis and secretion in cultured myofibroblasts, thus preventing the occurrence and expansion of cardiac fibrosis ( Figure 7).…”

Section: Cardioprotection By Kallistatin Via Antioxidation L Gao Et Almentioning

confidence: 54%

Role of kallistatin in prevention of cardiac remodeling after chronic myocardial infarction

Gao

Yin

Smith

et al. 2008

Laboratory Investigation

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Oxidative stress causes cardiomyocyte death and subsequent ventricular dysfunction and cardiac remodeling after myocardial infarction (MI), thus contributing to high mortality in chronic heart failure patients. We investigated the effects of kallistatin in cardiac remodeling in a chronic MI rat model and in primary cardiac cells. Human kallistatin gene was injected intramyocardially 20 min after ligation of the left coronary artery. At 4 weeks after MI, expression of human kallistatin in rat hearts was identified by reverse transcription-polymerase chain reaction, immunohistochemistry and ELISA. Kallistatin administration improved cardiac performance, increased mean arterial pressure, decreased myocardial infarct size and restored left ventricular wall thickness. Kallistatin treatment significantly attenuated cardiomyocyte size and atrial natriuretic peptide expression. Kallistatin also reduced collagen accumulation, collagen fraction volume and expression of collagen types I and III, transforming growth factor-b1 (TGF-b1) and plasminogen activator inhibitor-1 in the myocardium. Inhibition of cardiac hypertrophy and fibrosis by kallistatin was associated with increased cardiac nitric oxide (NO) levels and decreased superoxide formation, NADH oxidase activity and p22-phox expression. Moreover, in both primary cultured rat cardiomyocytes and myofibroblasts, recombinant kallistatin inhibited intracellular superoxide formation induced by H 2 O 2 , and the antioxidant effect of kallistatin was abolished by No-nitro-L-arginine methyl ester (L-NAME), indicating a NO-mediated event. Kallistatin promoted survival of cardiomyocytes subjected to H 2 O 2 treatment, and inhibited H 2 O 2 -induced Akt and ERK phosphorylation, as well as NF-kB activation. Furthermore, kallistatin abrogated TGF-b-induced collagen synthesis and secretion in cultured myofibroblasts. This is the first study to demonstrate that kallistatin improves cardiac performance and prevents post-MI-induced cardiac hypertrophy and fibrosis through its antioxidant action. Myocardial infarction (MI) leads to cardiac remodeling with complex structural alterations. After an ischemic insult, left ventricle (LV) enlargement is followed by progressive diastolic stiffness, enhanced wall stress and oxygen consumption, thus resulting in cardiomyocyte hypertrophy, interstitial fibrosis and decreased cardiac output. Increased reactive oxygen species (ROS) levels are recognized to be involved in ischemic heart failure and considered to be a major cause of cardiomyocyte death, ventricular dysfunction and heart failure progress. 1 Under pathological conditions, increased oxidative stress damages DNA and mitochondrial function, activates proapoptotic signaling kinases and leads to myocyte apoptosis or necrosis. 2,3 Elevation of ROS activates a series of hypertrophic signaling kinases and transcription factors to stimulate cardiac hypertrophy. 3,4 Moreover, ROS stimulate fibroblast proliferation and activate the expression of profibrotic factors, including transforming growth...

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“…Immunostaining of rat liver slices was performed as previously described. 23 Samples were incubated with anti-␣-SMA 141A (diluted 1:100, Sigma, St. Louis, MO) and anti-ILK (Upstate Biotechnology, Lake Placid, NY; diluted 1:100) antibodies. For immunofluorescence staining, HSCs were incubated first with an anti-ILK antibody, followed by incubation with both FITC-labeled anti-rabbit IgG and Cy3-labeled anti-␣-SMA 141A (diluted 1:100, Sigma, St. Louis, MO) antibodies.…”

Section: Methodsmentioning

confidence: 99%

Involvement of integrin-linked kinase in carbon tetrachloride–induced hepatic fibrosis in rats

et al. 2006

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Integrin-linked kinase (ILK) is a multidomain focal adhesion protein implicated in signal transduction between integrins and growth factor receptors. Although its expression is upregulated in pulmonary and renal fibrosis, its role in the development of hepatic fibrosis remains to be determined. Therefore, we considered it important to investigate whether ILK is involved in activation of hepatic stellate cells and thus plays a role in the development of hepatic fibrosis. Immunohistochemical analysis of liver sections obtained from rats with CCl 4 -induced cirrhosis revealed increased expression and colocalization of ILK and alpha-smooth muscle actin in hepatic stellate cells in perisinusoidal areas. In addition, hepatic stellate cells isolated from fibrotic livers expressed high levels of ILK and alpha-smooth muscle actin, and their expression was sustained in culture. In contrast, hepatic stellate cells (HSCs) isolated from normal rat liver did not express ILK, but its expression was increased when the cells were activated in culture. Our studies also showed that ILK is involved in the phosphorylation of ERK 1/2, p38 MAPK, JNK, and PKB and that selective inhibition of ILK expression by siRNA results in a significant decrease in their phosphorylation. These changes were accompanied by significant inhibition of cell spreading and migration without affecting cell proliferation. In conclusion, ILK plays a key role in HSC activation and could be a possible target for antifibrogenic therapy. (HEPATOLOGY 2006;44:612-622.)

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Taurine inhibits oxidative damage and prevents fibrosis in carbon tetrachloride-induced hepatic fibrosis

Cited by 95 publications

References 49 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

Role of kallistatin in prevention of cardiac remodeling after chronic myocardial infarction

Involvement of integrin-linked kinase in carbon tetrachloride–induced hepatic fibrosis in rats

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