Abstract
This study is to examine if hydrogen-rich saline reduced amyloid β (Aβ) induced neural inflammation, and learning and memory deficits in a rat model. S-D male rats (n = 84, 280-330 g) were divided into three groups, sham-operated, Aβ1-42 injected and Aβ1-42 plus hydrogen-rich saline-treated animals. Hydrogen-rich saline (5 ml/kg, i.p., daily) was injected for 14 days after intracerebroventricular injection of Aβ1-42. The levels of MDA, IL-6 and TNF-α were assessed by biochemical and ELISA analysis. Morris Water Maze and open field task were used to assess the memory dysfunction and motor dysfunction, respectively. LTP were used to detect the electrophysiology changes, HNE and GFAP immunohistochemistry were used to assess the oxidative stress and glial cell activation. After Aβ1-42 injection, the levels of MDA, IL-6, and TNF-α were increased in brain tissues and hydrogen-rich saline treatment suppressed MDA, IL-6, and TNF-α concentration. Hydrogen-rich saline treatment improved Morris Water Maze and enhanced LTP in hippocampus blocked by Aβ1-42. Furthermore, hydrogen-rich saline treatment also decreased the immunoreactivitiy of HNE and GFAP in hippocampus induced by Aβ1-42. In conclusion, hydrogen-rich saline prevented Aβ-induced neuroinflammation and oxidative stress, which may contribute to the improvement of memory dysfunction in this rat model. © 2010 Elsevier B.V. All rights reserved.
Original language | English |
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Pages (from-to) | 152-161 |
Number of pages | 10 |
Journal | Brain Research |
Volume | 1328 |
DOIs | |
State | Published - Apr 30 2010 |
ASJC Scopus Subject Areas
- General Neuroscience
- Molecular Biology
- Clinical Neurology
- Developmental Biology
Keywords
- Alzheimer's disease
- Amyloid
- Hydrogen
- Oxidative stress
- Free Radical Scavengers/pharmacology
- Alzheimer Disease/chemically induced
- Injections, Intraventricular
- Male
- Brain/drug effects
- Glial Fibrillary Acidic Protein
- Oxidative Stress/drug effects
- Peptide Fragments/antagonists & inhibitors
- Memory Disorders/chemically induced
- Hydrogen/pharmacology
- Sodium Chloride/pharmacology
- Disease Models, Animal
- Tumor Necrosis Factor-alpha/drug effects
- Encephalitis/chemically induced
- Rats
- Treatment Outcome
- Long-Term Potentiation/drug effects
- Rats, Sprague-Dawley
- Animals
- Interleukin-6/metabolism
- Maze Learning/drug effects
- Amyloid beta-Peptides/antagonists & inhibitors