ArticleWorld journal of gastroenterology2025
Characterization of hepatic pathology during azoxymethane-induced acute liver failure.
Article in World journal of gastroenterology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Animal models accurately representing acute liver failure (Review).International journal of molecular medicine · 2026Review
- Green-Synthesized Silver Nanoparticles from Garlic Peel Target NF-κB and Redox Imbalance: A Novel Therapeutic Strategy Against Pyrogallol-Induced Hepatotoxicity in Rats.Nanomaterials (Basel, Switzerland) · 2025Article
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Authors and funding
6 authors.
Funding
Abstract
backgroundAcute liver failure (ALF) is a loss of liver function due to a severe hepatic insult. Studies utilizing the azoxymethane (AOM) mouse model of ALF, which also generates hepatic encephalopathy, have primarily focused on development of neurological deficits. However, the molecular processes that generate liver damage have not been fully characterized. Therefore, a more comprehensive characterization of the hepatic consequences of AOM toxicity is needed to better understand this disease model.
aimTo identify molecular pathology contributing to hepatic injury during the progression of AOM-induced ALF.
methodsC57BL/6 mice were injected with AOM to produce ALF and hepatic encephalopathy. Tissue was collected at defined stages of neurological decline up to coma. Liver injury, CYP2E1 expression, oxidative stress, inflammation, apoptosis, necroptosis, and hepatocellular senescence were assessed.
resultsIncreased hepatic necrosis and exacerbated liver injury were observed after AOM injection as mice progressed towards coma. CYP2E1 expression decreased in AOM-treated mice as liver injury progressed. Malondialdehyde, myeloperoxidase and other measures of oxidative stress were significantly increased during AOM-induced ALF. Hepatic CCL2 and tumor necrosis factor α expression increased as AOM-induced liver injury progressed. Mixed lineage kinase domain-like protein phosphorylation was increased early during the progression of AOM-induced liver injury. Measures of apoptosis and cellular senescence all increased as the time course of AOM progressed.
conclusionThese data support that necrosis, oxidative stress, inflammation, apoptosis, and senescence were elevated in AOM-treated mice, with inflammation being the earliest significant change.
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