ArticleJournal of neuroinflammation2018
Effect of tumor necrosis factor-α on the expression of the ammonia transporter Rhcg in the brain in mice with acute liver failure.
Article in Journal of neuroinflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- The role of systemic inflammation in hepatic encephalopathy: advances in inflammatory mechanisms, prevention and treatment research.Annals of medicine · 2026Review
- Animal models accurately representing acute liver failure (Review).International journal of molecular medicine · 2026Review
- Edaravone reduces brain injury in hepatic encephalopathy by upregulation of Nrf2/HO-1 and inhibition of NF-κB, iNOS/NO and inflammatory cytokines.Molecular biology reports · 2025Article
- Article
- Feasibility exploration of GSH in the treatment of acute hepatic encephalopathy from the aspects of pharmacokinetics, pharmacodynamics, and mechanism.Frontiers in pharmacology · 2024Article
- Long Noncoding RNAs Regulate Hyperammonemia-Induced Neuronal Damage in Hepatic Encephalopathy.Oxidative medicine and cellular longevity · 2022Article
- ACSA-2 and GLAST classify subpopulations of multipotent and glial-restricted cerebellar precursors.Journal of neuroscience research · 2021Article
- Article
- Could protein content of Urinary Extracellular Vesicles be useful to detect Cirrhosis in Alcoholic Liver Disease?International journal of biological sciences · 2021Article
- Taurine transporter (TauT) deficiency impairs ammonia detoxification in mouse liver.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundAmmonia and tumor necrosis factor-alpha (TNF-α) play important roles in the mechanisms of hepatic encephalopathy (HE). Rhesus glycoprotein C (Rhcg) is important for ammonia transport especially in the kidney. The aim of the present study was to investigate the role of Rhcg in the brain in acute liver failure (ALF) and the effect of TNF-α on Rhcg expression.
methodsALF mouse models were generated by treatment with D-galactosamine (D-GalN) and lipopolysaccharide (LPS), or D-GalN and TNF-α. ALF induction was blocked by pretreatment with anti-TNF-α IgG. The levels of serum TNF-α were determined by ELISA. Blood ammonia and brain ammonia concentrations were detected using an ammonia assay kit. The expression and distribution of Rhcg in the brain tissues of ALF mice were examined by western blotting, real-time PCR, immunohistochemical, and immunofluorescence analyses.
resultsSerum TNF-α levels were increased in the LPS/D-GalN group. Blood and brain ammonia were increased in the LPS/D-GalN- and TNF-α/D-GalN-induced ALF groups. Rhcg mRNA and protein levels were elevated in both ALF groups, consistent with the increase in blood and brain ammonia. Rhcg was mainly expressed in vascular endothelial cells and astrocytes. Pretreatment with anti-TNF-α IgG antibody downregulated Rhcg in brain tissues in the LPS/D-GalN group, prevented the occurrence of ALF, and reduced blood and brain ammonia levels in the LPS/D-GalN group.
conclusionTNF-α promoted the transport of ammonia from the blood to brain tissues and exacerbated the toxic effects of ammonia by upregulating Rhcg.
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