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Metabolic Brain Disease

Erschienen in:

01.09.2010 | Original Paper

Brain expression of the water channels Aquaporin-1 and -4 in mice with acute liver injury, hyperammonemia and brain edema

verfasst von: Martin Eefsen, Peter Jelnes, Lars E. Schmidt, Ben Vainer, Hanne Cathrine Bisgaard, Fin S. Larsen

Erschienen in: Metabolic Brain Disease | Ausgabe 3/2010

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Abstract

Cerebral edema is a feared complication to acute liver failure (ALF), but the pathogenesis is still poorly understood. The water channels Aquaporin-1 (Aqp1) and -4 (Aqp4) has been associated with brain edema formation in several neuropathological conditions, indicating a possible role of Aqp1 and/or Aqp4 in ALF mediated brain edema. We induced acute liver injury and hyperammonemia in mice, to evaluate brain edema formation and the parallel expression of Aqp1 and Aqp4 in ALF. Liver injury and hyperammonemia were induced by +D-galactosamine (GLN) plus lipopolysaccharide (LPS) intraperitoneally and intravenous ammonia-acetate (NH₄ ⁺), the GLN+LPS+NH₄ ⁺ group. The vehicle control group (CONTROL) was treated with NaCl and phosphate-buffered saline. The GLN+LPS+NH₄ ⁺ group showed significantly elevated p-alanine aminotransferase, p-INR and p-ammonium vs. CONTROL (p < 0.001). Cortical brain water content was significantly elevated in the GLN+LPS+NH₄ ⁺ group vs. CONTROL, mean (SEM) 80.8(0.3) vs 80.0(0.1) % (p < 0.05). Western blot of membrane enriched cortical brain tissue showed significantly upregulation of Aqp4 in the GLN+LPS+NH₄ ⁺ group vs. CONTROL, mean AU (SEM) 100775(14820) vs. 58857(6266) (p < 0.05), and stationary levels for Aqp1. Aqp1 and Aqp4 mRNA were stationary. This study indicates that Aqp4, but not Aqp1, may be of importance in the pathogenesis of cortical brain edema in mice with ALF.

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Titel: Brain expression of the water channels Aquaporin-1 and -4 in mice with acute liver injury, hyperammonemia and brain edema
verfasst von: Martin Eefsen
Peter Jelnes
Lars E. Schmidt
Ben Vainer
Hanne Cathrine Bisgaard
Fin S. Larsen
Publikationsdatum: 01.09.2010
Verlag: Springer US
Erschienen in: Metabolic Brain Disease / Ausgabe 3/2010
Print ISSN: 0885-7490
Elektronische ISSN: 1573-7365
DOI: https://doi.org/10.1007/s11011-010-9213-y

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