Opioid-like compound exerts anti-fibrotic activity via decreased hepatic stellate cell activation and inflammation.

  title={Opioid-like compound exerts anti-fibrotic activity via decreased hepatic stellate cell activation and inflammation.},
  author={Stephani A Day and Ashley M. Lakner and Cathy C. Moore and M. H. Yen and Mark G. Clemens and Edwin Wu and Laura W Schrum},
  journal={Biochemical pharmacology},
  volume={81 8},

The Regulation of Lipid Metabolism by Targeting Opioid Receptors in Nonalcoholic Fatty Liver Disease

The pathogenesis of NAFLD can be improved by the modulation of opioid receptors to attenuate hepatic lipid abnormalities and the identification of potential compounds by targeting opioid receptors in the improvement ofNAFLD is promising.

Metabolic derivatives of alcohol and the molecular culprits of fibro-hepatocarcinogenesis: Allies or enemies?

This review examined published scientific findings on how alcohol and its metabolic derivatives mount cellular attack on each hepatic cell and the underlying molecular mechanisms leading to disruption of core hepatic homeostatic functions which probably set the stage for the initiation and progression of ALD to fibro-hepatocarcinogenesis.

Comparative Study between the Effect of Atorvastatin and Naltrexone on Hepatic Fibrosis Induced by Bile Duct Ligation in Rats

Naltrexone is more effective than atorvastatin in attenuation of BDL induced hepatic fibrosis and both could be of beneficial effects in treatment of liver fibrosis in clinical practice.

Erythrocytes Membrane Alterations Reflecting Liver Damage in CCl₄-Induced Cirrhotic Rats: The Ameliorative Effect of Naltrexone.

This study shows that the progression of liver cirrhosis and the ameliorative effect of NTX can be followed through alterations of these markers.

Strategies Targeting the Innate Immune Response for the Treatment of Hepatitis C Virus-Associated Liver Fibrosis

Current state-of-the-art knowledge on treatments targeting the innate immune system to revert chronic hepatitis C-associated liver fibrosis is discussed, with several drugs being tested in phase 2 and phase 3 trials with promising results.

Naltrexone prevents delayed encephalopathy in rats poisoned with the sarin analogue diisopropylflurophosphate.

A Case Report of Intrahepatic Cholangiocarcinoma in a Young Male

Although there is no case described in literature of CCA due to opioid consumption, hepatotoxic Heroin and Methadone exposition may have exerted a role on cholangiocytes proliferation, increasing proinflammatory and mutagenic stimuli and down-regulating local pro-apoptotic factors, leading ultimately to CCA development in this young patient.

Efeitos da capsaicina em células estreladas hepáticas

Essas descobertas mostram that a capsaicina tem potencial para ser um novo agente terapeutico no tratamento da fibrose hepatica devido a suas acoes antifibrogenicas e antiproliferativas.

Hepatoprotective Effects of Morchella esculenta against Alcohol-Induced Acute Liver Injury in the C57BL/6 Mouse Related to Nrf-2 and NF-κB Signaling

The hepatoprotective effects of Morchella esculenta fruit body against alcohol-induced acute liver injury were confirmed and the mechanism of action may be related to modulation of antioxidative and anti-inflammatory signaling pathways, partially via regulation of Nrf-2 and NF-κB signaling.



Naltrexone, an opioid receptor antagonist, attenuates liver fibrosis in bile duct ligated rats

This is the first study to demonstrate that administration of an opioid antagonist prevents the development of hepatic fibrosis in cirrhosis, and can influence liver fibrogenesis directly via the effect on HSCs and regulation of the redox sensitive mechanisms in the liver.

Role of endogenous opioids in modulating HSC activity in vitro and liver fibrosis in vivo

Endogenous opioids released during chronic liver injury participate in the process of liver fibrogenesis by stimulating HSC proliferation and collagen production in a paracrine manner.

TLR4 enhances TGF-β signaling and hepatic fibrosis

Modulation of TGF-β signaling by a TLR4-MyD88–NF-κB axis provides a novel link between proinflammatory and profibrogenic signals.

Endogenous opioids modulate the growth of the biliary tree in the course of cholestasis.

The increase in opioid peptide synthesis in the course of cholestasis aims to limit the excessive growth of the biliary tree in the Course of chollestasis by the interaction with the deltaOR expressed by cholangiocytes.

Toll‐Like receptor 4 mediates inflammatory signaling by bacterial lipopolysaccharide in human hepatic stellate cells

Human activated HSCs utilize components of TLR4 signal transduction cascade to stimulate NF‐κB and JNK and up‐regulate chemokines and adhesion molecules, and are a potential mediator of LPS‐induced liver injury.

IL‐6 induces hepatic inflammation and collagen synthesis in vivo

IL‐6 regulates the synthesis of a broad spectrum of acute phase proteins in the liver. Also, it is involved in the pathogenesis of many fibrogenic diseases. To study ihe inflammatory effects of IL‐6


Chronic ethanol feeding combined with LPS induces liver fibrosis, and the addition of SAMe significantly reduces hepatic injury and fibrosis through inhibition of oxidative stress and HSC activation.

New insights into the role of endogenous opioids in the pathogenesis of gastrointestinal and liver disease

The available data concerning the role of endogenous opioids in the pathophysiology of gastrointestinal and liver disease is examined and new therapeutic possibilities of opioid manipulation in gastrointestinal diseases are discussed.

TNFalpha is required for cholestasis-induced liver fibrosis in the mouse.