scholarly journals The secretin/secretin receptor axis modulates liver fibrosis through changes in transforming growth factor-β1 biliary secretion in mice

Hepatology ◽  
2016 ◽  
Vol 64 (3) ◽  
pp. 865-879 ◽  
Author(s):  
Nan Wu ◽  
Fanyin Meng ◽  
Pietro Invernizzi ◽  
Francesca Bernuzzi ◽  
Julie Venter ◽  
...  
Keyword(s):  
Growth Factor ◽  
Liver Fibrosis ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Biliary Secretion ◽  
Secretin Receptor

scholarly journals The Secretin/Secretin Receptor Axis Modulates Ductular Reaction and Liver Fibrosis through Changes in Transforming Growth Factor-β1–Mediated Biliary Senescence

2018 ◽  
Vol 188 (10) ◽  
pp. 2264-2280 ◽  
Author(s):  
Nan Wu ◽  
Fanyin Meng ◽  
Tianhao Zhou ◽  
Julie Venter ◽  
Thao K. Giang ◽  
...  
Keyword(s):  
Growth Factor ◽  
Liver Fibrosis ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Ductular Reaction ◽  
Secretin Receptor

Association of polymorphisms of the transforming growth factor-β1 gene with the rate of progression of HCV-induced liver fibrosis

2002 ◽  
Vol 316 (1-2) ◽  
pp. 83-94 ◽  
Author(s):  
Jan Gewaltig ◽  
Kerstin Mangasser-Stephan ◽  
Carsten Gartung ◽  
Stefan Biesterfeld ◽  
Axel M Gressner
Keyword(s):  
Growth Factor ◽  
Liver Fibrosis ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Rate Of Progression

scholarly journals Therapeutic Effects of an Inhibitor of Thioredoxin Reductase on Liver Fibrosis by Inhibiting the Transforming Growth Factor-β1/Smads Pathway

2021 ◽  
Vol 8 ◽  
Author(s):  
Wenxuan Jiao ◽  
Man Bai ◽  
Hanwei Yin ◽  
Jiayi Liu ◽  
Jing Sun ◽  
...  
Keyword(s):  
Growth Factor ◽  
Liver Fibrosis ◽  
Molecular Mechanisms ◽  
Transforming Growth Factor ◽  
Smooth Muscle Actin ◽  
Thioredoxin Reductase ◽  
Transforming Growth Factor Β1 ◽  
Therapeutic Effects ◽  
Pathological State ◽  
Tgf Β1

Liver fibrosis is an important stage in the progression of liver injury into cirrhosis or even liver cancer. Hepatic stellate cells (HSCs) are induced by transforming growth factor-β1 (TGF-β1) to produce α-smooth muscle actin (α-SMA) and collagens in liver fibrosis. Butaselen (BS), which was previously synthesized by our group, is an organic selenium compound that exerts antioxidant and tumor cell apoptosis–promoting effects by inhibiting the thioredoxin (Trx)/thioredoxin reductase (TrxR) system. The aim of this study was to investigate the potential effects of BS on liver fibrosis and explore the underlying molecular mechanisms of its action. Liver fibrosis models were established using male BALB/c mice through intraperitoneal injection of CCl4. BS was administered orally once daily at a dose of 36, 90, or 180 mg/kg. Silymarin (Si), which is a drug used for patients with nonalcoholic fatty liver disease and nonalcoholic steatohepatitis, was administered at a dose of 30 mg/kg per day as a control. The action mechanisms of BS against liver fibrosis progression were examined in HSCs. The study revealed that the activity and expression levels of TrxR were elevated in the mouse liver and serum after CCl4-induced liver fibrosis. Oral administration of BS relieved the pathological state of mice with liver fibrosis, showing significant therapeutic effects against liver fibrosis. Moreover, BS not only induced HSC apoptosis but also inhibited the production of α-SMA and collagens by HSCs by downregulating the TGF-β1 expression and blocking the TGF-β1/Smads pathway. The results of the study indicated that BS inhibited liver fibrosis by regulating the TGF-β1/Smads pathway.

Inhibition of liver fibrosis by solubilized coenzyme Q10: Role of Nrf2 activation in inhibiting transforming growth factor-β1 expression

2009 ◽  
Vol 240 (3) ◽  
pp. 377-384 ◽  
Author(s):  
Hoo-Kyun Choi ◽  
Yuba Raj Pokharel ◽  
Sung Chul Lim ◽  
Hyo-Kyung Han ◽  
Chang Seon Ryu ◽  
...  
Keyword(s):  
Growth Factor ◽  
Liver Fibrosis ◽  
Coenzyme Q10 ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Nrf2 Activation ◽  
Inhibition Of Liver Fibrosis

Contribution of sinusoidal endothelial liver cells to liver fibrosis: Expression of transforming growth factor-β1 receptors and modulation of plasmin-generating enzymes by transforming growth factor-β1

Hepatology ◽  
1993 ◽  
Vol 18 (4) ◽  
pp. 937-944 ◽  
Author(s):  
Hartmut Rieder ◽  
Thomas Armbrust ◽  
Karl-Hermann Meyer zum Büschenfelde ◽  
Giuliano Ramadori
Keyword(s):  
Growth Factor ◽  
Liver Fibrosis ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Liver Cells

scholarly journals Aqueous Date Flesh or Pits Extract Attenuates Liver Fibrosis via Suppression of Hepatic Stellate Cell Activation and Reduction of Inflammatory Cytokines, Transforming Growth Factor-β1 and Angiogenic Markers in Carbon Tetrachloride-Intoxicated Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-19 ◽  
Author(s):  
Nouf M. Al-Rasheed ◽  
Hala A. Attia ◽  
Raeesa A. Mohamad ◽  
Nawal M. Al-Rasheed ◽  
Maha A. Al-Amin ◽  
...  
Keyword(s):  
Growth Factor ◽  
Liver Fibrosis ◽  
Inflammatory Cytokines ◽  
Cell Activation ◽  
Transforming Growth Factor ◽  
Stellate Cell ◽  
Smooth Muscle Actin ◽  
Interleukin 1 ◽  
Transforming Growth Factor Β1 ◽  
Angiogenic Markers

Previous data indicated the protective effect of date fruit extract on oxidative damage in rat liver. However, the hepatoprotective effects via other mechanisms have not been investigated. This study was performed to evaluate the antifibrotic effect of date flesh extract (DFE) or date pits extract (DPE) via inactivation of hepatic stellate cells (HSCs), reducing the levels of inflammatory, fibrotic and angiogenic markers. Coffee was used as reference hepatoprotective agent. Liver fibrosis was induced by injection of CCl4(0.4 mL/kg) three times weekly for 8 weeks. DFE, DPE (6 mL/kg), coffee (300 mg/kg), and combination of coffee + DFE and coffee + DPE were given to CCl4-intoxicated rats daily for 8 weeks. DFE, DPE, and their combination with coffee attenuated the elevated levels of inflammatory cytokines including tumor necrosis factor-α, interleukin-6, and interleukin-1β. The increased levels of transforming growth factor-β1 and collagen deposition in injured liver were alleviated by both extracts. CCl4-induced expression ofα-smooth muscle actin was suppressed indicating HSCs inactivation. Increased angiogenesis was ameliorated as revealed by reduced levels and expression of vascular endothelial growth factor and CD31. We concluded that DFE or DPE could protect liver via different mechanisms. The combination of coffee with DFE or DPE may enhance its antifibrotic effects.

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