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

Bibliographic Details
Title: 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
Authors: Dalia Mahmoud Abdelmonem Elsherbini, Fatma M. Ghoneim, Eman Mohammed El-Mancy, Hasnaa Ali Ebrahim, Mohamed El-Sherbiny, Mohamed El-Shafey, Rasha Hamed Al-Serwi, Nehal M. Elsherbiny
Source: Frontiers in Cellular Neuroscience, Vol 16 (2022)
Publisher Information: Frontiers Media S.A., 2022.
Publication Year: 2022
Collection: LCC:Neurosciences. Biological psychiatry. Neuropsychiatry
Subject Terms: GFAP, inwardly rectifying potassium channel, brain edema, aquaporin-4, TNFα, Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571
More Details: 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.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 1662-5102
Relation: https://www.frontiersin.org/articles/10.3389/fncel.2022.896172/full; https://doaj.org/toc/1662-5102
DOI: 10.3389/fncel.2022.896172
Access URL: https://doaj.org/article/4c35236ba0984f5f99eefa462b411273
Accession Number: edsdoj.4c35236ba0984f5f99eefa462b411273
Database: Directory of Open Access Journals
More Details
ISSN:16625102
DOI:10.3389/fncel.2022.896172
Published in:Frontiers in Cellular Neuroscience
Language:English