Abstract
This study is to examine if hydrogen-rich saline reduced amyloid-beta (Aβ) induced neural inflammation and oxidative stress in a rat model by attenuation of activation of JNK and NF-κB. Sprague-Dawley male rats (n=18, 280-330g) were divided into three groups, sham operated, Aβ1-42 injected and Aβ1-42 plus hydrogen-rich saline treated animals. Hydrogen-rich saline (5ml/kg, i.p., daily) was injected for 10 days after intraventricular injection of Aβ1-42. The levels of IL-1β were assessed by ELISA analysis, 8-OH-dG by immunohistochemistry in the brain slides, and JNK and NF-κB by immunohistochemistry and western blotting. After Aβ1-42 injection, the level of IL-1β, 8-OH-dG, JNK and NF-κB all increased in brain tissues, while hydrogen-rich saline treatment decreased the level of IL-1β, 8-OH-dG and the activation of JNK and NF-κB. In conclusion, hydrogen-rich saline prevented Aβ-induced neuroinflammation and oxidative stress, possibly by attenuatation of activation of c-Jun NH2-terminal kinase (JNK) and nuclear factor-κB (NF-κB) in this rat model. © 2011 Elsevier Ireland Ltd.
Original language | English |
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Pages (from-to) | 127-132 |
Number of pages | 6 |
Journal | Neuroscience Letters |
Volume | 491 |
Issue number | 2 |
DOIs | |
State | Published - Mar 17 2011 |
ASJC Scopus Subject Areas
- General Neuroscience
Keywords
- Alzheimer's disease
- Amyloid-beta
- Hydrogen
- JNK
- NF-κB
- Oxidative stress
- Immunohistochemistry
- Inflammation/enzymology
- Enzyme Activation/drug effects
- Free Radical Scavengers/pharmacology
- Rats
- Male
- Rats, Sprague-Dawley
- Brain/drug effects
- Oxidative Stress/drug effects
- Animals
- Amyloid beta-Peptides/toxicity
- Hydrogen/pharmacology
- MAP Kinase Kinase 4/antagonists & inhibitors
- NF-kappa B/antagonists & inhibitors
- Alzheimer Disease/metabolism
- Sodium Chloride/pharmacology
- Disease Models, Animal