Sequential behaviour of extracellular matrix glycoproteins in an experimental model of hepatic fibrosis

1985 ◽  
Vol 49 (1) ◽  
pp. 317-324 ◽  
Author(s):  
G. Ballardini ◽  
A. Faccani ◽  
M. Fallani ◽  
S. Berti ◽  
V. Vasi ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Experimental Model ◽  
Hepatic Fibrosis ◽  
Sequential Behaviour

scholarly journals Natural Sulfur-Containing Compounds: An Alternative Therapeutic Strategy against Liver Fibrosis

Cells ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 1356 ◽  
Author(s):  
Milito ◽  
Brancaccio ◽  
D’Argenio ◽  
Castellano
Keyword(s):  
Extracellular Matrix ◽  
Growth Factor ◽  
Liver Fibrosis ◽  
Hepatic Fibrosis ◽  
Molecular Mechanisms ◽  
Transforming Growth Factor ◽  
Extracellular Matrix Proteins ◽  
Matrix Proteins ◽  
Sulfur Containing ◽  
Sulfur Containing Compounds

Liver fibrosis is a pathophysiologic process involving the accumulation of extracellular matrix proteins as collagen deposition. Advanced liver fibrosis can evolve in cirrhosis, portal hypertension and often requires liver transplantation. At the cellular level, hepatic fibrosis involves the activation of hepatic stellate cells and their transdifferentiation into myofibroblasts. Numerous pro-fibrogenic mediators including the transforming growth factor-β1, the platelet-derived growth factor, endothelin-1, toll-like receptor 4, and reactive oxygen species are key players in this process. Knowledge of the cellular and molecular mechanisms underlying hepatic fibrosis development need to be extended to find novel therapeutic strategies. Antifibrotic therapies aim to inhibit the accumulation of fibrogenic cells and/or prevent the deposition of extracellular matrix proteins. Natural products from terrestrial and marine sources, including sulfur-containing compounds, exhibit promising activities for the treatment of fibrotic pathology. Although many therapeutic interventions are effective in experimental models of liver fibrosis, their efficacy and safety in humans are largely unknown. This review aims to provide a reference collection on experimentally tested natural anti-fibrotic compounds, with particular attention on sulfur-containing molecules. Their chemical structure, sources, mode of action, molecular targets, and pharmacological activity in the treatment of liver disease will be discussed.

scholarly journals Pathogenesis of hepatic septal fibrosis associated with Capillaria hepatica infection of rats

2001 ◽  
Vol 34 (6) ◽  
pp. 503-506 ◽  
Author(s):  
Antônio Benigno dos Santos ◽  
Miguel Tolentino Junior ◽  
Zilton A. Andrade
Keyword(s):  
Experimental Model ◽  
Hepatic Fibrosis ◽  
Liver Parenchyma ◽  
Hepatica Infection ◽  
Capillaria Hepatica ◽  
Factors Associated ◽  
Mild Degree ◽  
Future Search ◽  
Focal Fibrosis

Septal fibrosis is a common form of hepatic fibrosis, but its etiology and pathogenesis are poorly understood. Rats infected with the helminth Capillaria hepatica constitute a good experimental model of such fibrosis. To investigate the pathogenetic contribution of the several parasitic factors involved, the following procedures were performed in rats: a) regarding the role of eggs, these were isolated and injected either into the peritoneal cavity or directly into the liver parenchyma; b) for worms alone, 15-day-old infection was treated with mebendazole, killing the parasites before oviposition started; c) for both eggs and worms, rats at the 30th day of infection were treated with either mebendazole or ivermectin. Eggs only originated focal fibrosis from cicatricial granulomas, but no septal fibrosis. Worms alone induced a mild degree of perifocal septal fibrosis. Systematized septal fibrosis of the liver, similar to that observed in the infected controls, occurred only in the rats treated with mebendazole or ivermectin, with dead worms and immature eggs in their livers. Thus, future search for fibrogenic factors associated with C. hepatica infection in rats should consider lesions with both eggs and worms.

scholarly journals Beta-arrestin2 deficiency protects against hepatic fibrosis in mice and prevents synthesis of extracellular matrix

2018 ◽  
Vol WCP2018 (0) ◽  
pp. PO2-6-4
Author(s):  
Wu-Yi Sun ◽  
Yuan-Jing Gu ◽  
Xin-Ran Li ◽  
Wen-Ting Peng ◽  
Jing-Yu Chen ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Hepatic Fibrosis

Acupuncture Combined with Curcumin Disrupts Platelet-Derived Growth Factor β Receptor/Extracellular Signal-Regulated Kinase Signalling and Stimulates Extracellular Matrix Degradation in Carbon Tetrachloride-Induced Hepatic Fibrosis in Rats

2012 ◽  
Vol 30 (4) ◽  
pp. 324-330 ◽  
Author(s):  
Xiao-Ping Zhang ◽  
Feng Zhang ◽  
Zi-Li Zhang ◽  
Jin Ma ◽  
De-Song Kong ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Carbon Tetrachloride ◽  
Growth Factor ◽  
Hepatic Fibrosis ◽  
Combination Treatment ◽  
Acupuncture Treatment ◽  
Platelet Derived Growth Factor ◽  
Fibrotic Liver ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal

Background Acupuncture treatment has been increasingly used to treat chronic liver diseases. We previously reported that acupuncture combined with curcumin, a natural antifibrotic compound, could remarkably attenuate liver fibrosis in chemically intoxicated rats, but the underlying molecular mechanisms are poorly understood. The present study was aimed at investigating the effects of acupuncture combined with curcumin on platelet-derived growth factor (PDGF) signalling and extracellular matrix (ECM) regulation in the fibrotic liver. Methods A total of 60 Sprague-Dawley male rats were randomly divided into control, model, sham, acupuncture, curcumin and combination treatment groups. During the establishment of fibrosis using carbon tetrachloride (CCl4), acupuncture at LR3, LR14, BL18 and ST36 and/or curcumin treatment by mouth were performed simultaneously. After treatment, serum PDGF levels were measured. Protein and mRNA expression of key effectors in PDGF pathway and fibrinolysis in the liver was determined. Results Acupuncture combined with curcumin potently reduced serum PDGF levels and selectively disrupted the PDGF-βR/extracellular signal-regulated kinase (ERK) cascade. Combination treatment also significantly repressed expression of connective tissue growth factor and upregulated expression of matrix metalloproteinase-9, promoting fibrinolysis in the fibrotic liver. Conclusions The beneficial effects of acupuncture and its combination with curcumin could be attributed to the disruption of PDGF-βR/ERK pathway and stimulated ECM degradation in the fibrotic liver. Acupuncture treatment significantly enhanced curcumin effects at the molecular level. These findings may provide molecular insights into the potential of acupuncture combined with curcumin for prevention of hepatic fibrosis.

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