ArticleFrontiers in cellular neuroscience2022
Astrocytes profiling in acute hepatic encephalopathy: Possible enrolling of glial fibrillary acidic protein, tumor necrosis factor-alpha, inwardly rectifying potassium channel (Kir 4.1) and aquaporin-4 in rat cerebral cortex.
Article in Frontiers in cellular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed.
- Neuroprotective effects of zingerone on the thioacetamide-induced hepatic encephalopathy in rats. Insights from oxidative stress, ER stress, BDNF signaling and apoptosis.Journal of molecular histology · 2026Article
- Toxic Alpha-Synuclein and the Opening of the Gate: Blood-Brain Barrier Damage and Stepwise Leukocyte Infiltration.Cellular and molecular neurobiology · 2026Review
- Impact of agmatine on cerebral astrocyte reactivity, neurodegeneration, and oxidative stress in bile duct-ligated rats.Metabolic brain disease · 2025Article
- Treatment with hydrogen-rich water protects against thioacetamide-induced hepatic encephalopathy in rats through stabilizing liver-brain disturbance.Scientific reports · 2025Article
- Role of glia in delirium: proposed mechanisms and translational implications.Molecular psychiatry · 2025Review
- Combination of Luteolin and Silibinin Has Hepatoprotective Effects on Rats' Liver Fibrosis Induced by Thioacetamide.Current drug delivery · 2025Article
- Role of aquaporins in brain water transport and edema.Frontiers in neuroscience · 2025Review
- The Role of Neuroinflammation in the Pathogenesis of Hepatic Encephalopathy.Journal of immunology research · 2025Review
- Neuronal injury and hepatotoxicity: astrocytes and stellate cells convergence and their role in tissue repair.Frontiers in neuroscience · 2025Review
- Hepatic encephalopathy as a result of ammonia-induced increase in GABAergic tone with secondary reduced brain energy metabolism.Metabolic brain disease · 2024Review
- Bibliometrics and knowledge mapping of the pathogenesis of hepatic encephalopathy in patients with liver cirrhosis.Heliyon · 2024Article
- Review
- Ammonium chloride reduces excitatory synaptic transmission onto CA1 pyramidal neurons of mouse organotypic slice cultures.Frontiers in cellular neuroscience · 2024Article
- Astrocyte regulation of extracellular space parameters across the sleep-wake cycle.Frontiers in cellular neuroscience · 2024Review
- Cellular Pathogenesis of Hepatic Encephalopathy: An Update.Biomolecules · 2023Review
- Yigan Mingmu Decoction inhibits diabetic macular edema through regulating Kir4.1/AQP4 axis: a study based on network pharmacology.American journal of translational research · 2023Article
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8 authors.
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Abstract
Hepatic encephalopathy (HE) is a neurological disarray manifested as a sequel to chronic and acute liver failure (ALF). A potentially fatal consequence of ALF is brain edema with concomitant astrocyte enlargement. This study aims to outline the role of astrocytes in acute HE and shed light on the most critical mechanisms driving this role. Rats were allocated into two groups. Group 1, the control group, received the vehicle. Group 2, the TAA group, received TAA (300 mg/kg) for 3 days. Serum AST, ALT, and ammonia were determined. Liver and cerebral cortical sections were processed for hematoxylin and eosin staining. Additionally, mRNA expression and immunohistochemical staining of cortical GFAP, TNFα, Kir4.1, and AQP4 were performed. Cortical sections from the TAA group demonstrated neuropil vacuolation and astrocytes enlargement with focal gliosis. GFAP, TNFα, and AQP4 revealed increased mRNA expression, positive immunoreactivity, and a positive correlation to brain water content. In contrast, Kir 4.1 showed decreased mRNA expression and immunoreactivity and a negative correlation to brain water content. In conclusion, our findings revealed altered levels of TNFα, Kir 4.1, GFAP, and AQP4 in HE-associated brain edema. A more significant dysregulation of Kir 4.1 and TNFα was observed compared to AQP4 and GFAP.
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