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Updated: May 12, 2026

Generation of a Rat Model of Acute Liver Failure by Combining 70% Partial Hepatectomy and Acetaminophen

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Published on: November 27, 2019

Inflammation and hepatic encephalopathy.

Iona Coltart¹, Thomas H Tranah, Debbie L Shawcross

¹Institute of Liver Studies, King's College London School of Medicine at King's College Hospital, King's College Hospital, Denmark Hill, London SE5 9RS, United Kingdom.

Archives of Biochemistry and Biophysics

|April 16, 2013

Summary

This summary is machine-generated.

Hepatic encephalopathy (HE) involves ammonia and inflammation, impacting brain function. This review explores their synergy and potential anti-inflammatory treatments for HE management.

Keywords:

Ammonia Hepatic encephalopathy Infection Inflammation Systemic inflammatory response syndrome

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Generation of a Rat Model of Acute Liver Failure by Combining 70% Partial Hepatectomy and Acetaminophen

Generation of a Rat Model of Acute Liver Failure by Combining 70% Partial Hepatectomy and Acetaminophen

Published on: November 27, 2019

Long Term Intravital Multiphoton Microscopy Imaging of Immune Cells in Healthy and Diseased Liver Using CXCR6.Gfp Reporter Mice

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Published on: March 24, 2015

Area of Science:

Neuroscience
Hepatology
Immunology

Background:

Hepatic encephalopathy (HE) is a neuropsychiatric syndrome linked to liver dysfunction.
Ammonia is a key factor, but inflammation significantly worsens neurological effects in HE.
Inflammation can be intrinsic to the brain or systemic, affecting the brain via mediators.

Purpose of the Study:

To review the synergistic relationship between ammonia and inflammation in HE pathogenesis.
To discuss sources of inflammation, including liver issues, bacterial translocation, and sepsis.
To overview current and emerging treatments targeting inflammation for HE prophylaxis and treatment.

Main Methods:

Literature review of studies on HE, ammonia, inflammation, and treatment.

Main Results:

Ammonia and inflammation synergistically contribute to HE manifestation.
Inflammation originates from liver damage, gut-derived endotoxins, and sepsis.
Existing and novel anti-inflammatory therapies show promise for HE.

Conclusions:

Inflammation plays a critical role alongside ammonia in HE.
Targeting inflammation offers a promising therapeutic strategy for HE.
Further research into anti-inflammatory treatments is warranted for clinical application in HE.