The N-Terminal Propeptide of Collagen Type III in Serum Reflects Activity and Degree of Fibrosis in Patients with Chronic Liver Disease†

Frei, Alain; Zimmermann, Arthur; Weigand, K.

doi:10.1002/hep.1840040505

Cited by 172 publications

(45 citation statements)

References 16 publications

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“…The sample was then embedded in paraffin, sliced into 5-μ m sections and stained with hematoxylin-eosin, followed by blinded histological assessment. The degree of portal inflammation, hepatocellular necrosis, and inflammatory cell infiltration was evaluated (19). The histological changes were evaluated in non-consecutive, randomly chosen × 200 histological fields.…”

Section: Histological Analysismentioning

confidence: 99%

Hepatoprotective Effect of Pinoresinol on Carbon Tetrachloride–Induced Hepatic Damage in Mice

et al. 2010

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Abstract. Forsythiae Fructus is known to have diuretic, anti-bacterial, and anti-inflammatory activities. This study examined the hepatoprotective effects of pinoresinol, a lignan isolated from Forsythiae Fructus, against carbon tetrachloride (CCl 4 )-induced liver injury. Mice were treated intraperitoneally with vehicle or pinoresinol (25, 50, 100, and 200 mg/kg) 30 min before and 2 h after CCl 4 (20 μ l/kg) injection. In the vehicle-treated CCl 4 group, serum aminotransferase activities were significantly increased 24 h after CCl 4 injection, and these increases were attenuated by pinoresinol at all doses. Hepatic glutathione contents were significantly decreased and lipid peroxidation was increased after CCl 4 treatment. These changes were attenuated by 50 and 100 mg/kg of pinoresinol. The levels of protein and mRNA expression of inflammatory mediators, including tumor necrosis factor-α , inducible nitric oxide synthase, and cyclooxygenase-2, were significantly increased after CCl 4 injection; and these increases were attenuated by pinoresinol. Nuclear translocation of nuclear factor-κ B (NF-κ B) and phosphorylation of c-Jun, one of the components of activating protein 1 (AP-1), were inhibited by pinoresinol. Our results suggest that pinoresinol ameliorates CCl 4 -induced acute liver injury, and this protection is likely due to antioxidative activity and down-regulation of inflammatory mediators through inhibition of NF-κ B and AP-1.

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Section: Histological Analysismentioning

confidence: 99%

Hepatoprotective Effect of Pinoresinol on Carbon Tetrachloride–Induced Hepatic Damage in Mice

et al. 2010

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“…Liver sections were stained with hematoxylin and eosin (H&E) and evaluated with light microscopy. The incidence and the degree of liver fibrosis, necrosis, fatty degeneration and inflammatory cell infiltrate were scored as normal (0), slight (1), moderate (2) or severe (3) (Frei et al, 1984).…”

Section: Pathological Examinationmentioning

confidence: 99%

Recombinant bovine pancreatic trypsin inhibitor protects the liver from carbon tetrachloride-induced chronic injury in rats

Dong¹,

Lv²,

Wang

et al. 2013

Pharmaceutical Biology

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(2013) Recombinant bovine pancreatic trypsin inhibitor protects the liver from carbon tetrachloride-induced chronic injury in rats, Pharmaceutical Biology, 51:10, 1298-1303, DOI: 10.3109/13880209.2013 Context: Bovine pancreatic trypsin inhibitor (BPTI) has been reported to relieve liver ischemiareperfusion-induced injury in rats. Objective: This study was designed to determine whether the recombinant BPTI (rBPTI) can prevent the chronic liver injury induced by CCl 4 in rats. Materials and methods: Fifty male Wistar rats were divided into five groups. Rats were treated with 40% CCl 4 at a dose of 2 ml/kg body weight twice a week subcutaneously for 12 weeks. In the 8th week, they were administered intraperitoneally with rBPTI (80 MU/kg), BPTI (80 MU/kg) or hepatocyte growth-promoting factor (pHGF; 100 mg/kg) daily for the next 4 weeks. Results: rBPTI significantly prevented the disruption of liver function of alanine aminotransferase (ALT; 172.7 AE 18.16 versus 141.2 AE 15.28, p ¼ 0.003), aspartate aminotransferase (AST; 225.10 AE 36.54 versus 170.06 AE 27.14, p ¼ 0.007) and hydroxyproline (Hyp; 1.14 AE 0.27 versus 0.62 AE 0.17, p ¼ 0.001). rBPTI significantly decreased the level of thiobarbituric acid reactive substances (TBARS; 1.15 AE 0.16 versus 0.87 AE 0.15, p ¼ 0.003) and increased the activities of superoxide dismutase (SOD; 6.07 AE 0.95 versus 7.75 AE 1.12, p ¼ 0.007). rBPTI reduced the production of cytokines of IL-1b and TGF-b. The hepatocyte necrosis, fibrosis, fatty degeneration and inflammatory cell infiltration were ameliorated by rBPTI administration. Conclusion: This study demonstrated that rBPTI exerted a hepatoprotective effect on chronic liver fibrosis induced by CCl 4 , which suggests that rBPTI may have the potential application for chronic liver injury induced by drugs metabolism and toxic substances.

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“…Samples were then embedded in paraffin, sliced into 5 μm sections, stained with hematoxylin-eosin, followed by blinded histological assessment. The degree of portal inflammation, hepatocellular necrosis, and inflammatory cell infiltration was evaluated (Frei et al, 1984). Histological changes were evaluated in non-consecutive, randomly chosen x 400 histological fields.…”

Section: Histological Analysismentioning

confidence: 99%

Protective Effects of Moutan Cortex Radicis against Acute Hepatotoxicity

Park

Kim

Lee

2011

Afr. J. Trad. Compl. Alt. Med.

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This study evaluated the potential beneficial effect of Moutan Cortex Radicis (MCR) in a murine model of carbon tetrachloride (CCl 4 )-, D-galactosamine (GalN)-and α-naphthylisothiocyanate (ANIT)-induced liver injury. Acute hepatotoxicity was induced by intraperitoneal injection of CCl 4 (10 μL/kg), GalN (700 mg/kg), and ANIT (40 mg/kg). Animals received MCR (30, 100, and 300 mg/kg ) orally at 48, 24, and 2 h before and 6 h after administration of CCl 4, GalN, and ANIT. Serum activities of aminotransferase were significantly higher at 24 h after CCl 4 or GalN treatment. These changes were attenuated by MCR. Histopathological analysis revealed multiple and extensive areas of portal inflammation, hepatocellular necrosis, and an increase in inflammatory cell infiltration. These changes were inhibited by MCR. Serum total bilirubin concentration increased and bile flow decreased significantly 48 h after ANIT treatment, which was attenuated by MCR. Our results suggest that MCR has a protective effect on acute liver injury.

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The N-Terminal Propeptide of Collagen Type III in Serum Reflects Activity and Degree of Fibrosis in Patients with Chronic Liver Disease†

Cited by 172 publications

References 16 publications

Hepatoprotective Effect of Pinoresinol on Carbon Tetrachloride–Induced Hepatic Damage in Mice

Hepatoprotective Effect of Pinoresinol on Carbon Tetrachloride–Induced Hepatic Damage in Mice

Recombinant bovine pancreatic trypsin inhibitor protects the liver from carbon tetrachloride-induced chronic injury in rats

Protective Effects of Moutan Cortex Radicis against Acute Hepatotoxicity

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