ArticleScientific reports2022
A mouse model of hepatic encephalopathy: bile duct ligation induces brain ammonia overload, glial cell activation and neuroinflammation.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- GUT MICROBIOTA ALTERATIONS IN RODENT MODELS OF CHOLESTASIS INDUCED BY BILE DUCT LIGATION: A SYSTEMATIC REVIEW.Arquivos de gastroenterologia · 2026Pooled it
- Adiponectin Inhibits Oxidative Stress and Tight Junction Protein Loss: Evidence from a Hepatic Encephalopathy Mouse Model and Brain Endothelial Cells.Pharmaceuticals (Basel, Switzerland) · 2026Article
- S100B in brain-gut-liver crosstalk: from glial activation to multiorgan inflammation.Frontiers in immunology · 2026Review
- Combining sorafenib andIranian journal of basic medical sciences · 2026Article
- Protective effect of artichoke (Cynara scolymus L.) leaf and receptaculum extracts against hepatic encephalopathy in bile duct ligated rats.Metabolic brain disease · 2025Article
- The Change of Noncoding RNA Expression in Olfactory Bulb of Hepatic Encephalopathy Mouse Model: Transcriptomic Analysis and Cellular Analysis.CNS neuroscience & therapeutics · 2025Article
- Article
- Activation of glutamine synthetase (GS) as a new strategy for the treatment of major depressive disorder and other GS-related diseases.Acta pharmacologica Sinica · 2025Article
- Dysregulation of bile acid signal transduction causes neurological dysfunction in cirrhosis rats.World journal of hepatology · 2025Article
- MEOX1-mediated transcriptional regulation of circABHD3 exacerbates hepatic fibrosis through promoting m6A/YTHDF2-dependent YPEL3 mRNA decay to activate β-catenin signaling.PLoS genetics · 2025Article
- Linking Brain and Immune Transcriptomes to Gut-Derived Metabolites in Hepatic Encephalopathy: An Explorative Integrative Multi-Omics Approach.Hepatic medicine : evidence and research · 2025Article
- Activation of the kynurenine pathway identified in individuals with covert hepatic encephalopathy.Hepatology communications · 2024Article
- Review
- Ammonium chloride reduces excitatory synaptic transmission onto CA1 pyramidal neurons of mouse organotypic slice cultures.Frontiers in cellular neuroscience · 2024Article
- Article
- Gut Microbiota and Neuroinflammation in Acute Liver Failure and Chronic Liver Disease.Metabolites · 2023Review
- Experimental hepatic encephalopathy causes early but sustained glial transcriptional changes.Journal of neuroinflammation · 2023Article
- Review
- Limitations of PLX3397 as a microglial investigational tool: peripheral and off-target effects dictate the response to inflammation.Frontiers in immunology · 2023Article
- Transcriptome Profile in the Mouse Brain of Hepatic Encephalopathy and Alzheimer's Disease.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatic encephalopathy (HE) is a common complication of chronic liver disease, characterized by an altered mental state and hyperammonemia. Insight into the brain pathophysiology of HE is limited due to a paucity of well-characterized HE models beyond the rat bile duct ligation (BDL) model. Here, we assess the presence of HE characteristics in the mouse BDL model. We show that BDL in C57Bl/6j mice induces motor dysfunction, progressive liver fibrosis, liver function failure and hyperammonemia, all hallmarks of HE. Swiss mice however fail to replicate the same phenotype, underscoring the importance of careful strain selection. Next, in-depth characterisation of metabolic disturbances in the cerebrospinal fluid of BDL mice shows glutamine accumulation and transient decreases in taurine and choline, indicative of brain ammonia overload. Moreover, mouse BDL induces glial cell dysfunction, namely microglial morphological changes with neuroinflammation and astrocyte reactivity with blood-brain barrier (BBB) disruption. Finally, we identify putative novel mechanisms involved in central HE pathophysiology, like bile acid accumulation and tryptophan-kynurenine pathway alterations. Our study provides the first comprehensive evaluation of a mouse model of HE in chronic liver disease. Additionally, this study further underscores the importance of neuroinflammation in the central effects of chronic liver disease.
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