Hydrogen-rich saline reduces oxidative stress and inflammation by inhibit of JNK and NF-κB activation in a rat model of amyloid-beta-induced Alzheimer's disease

Cai Wang, Jian Li, Qiang Liu, Rui Yang, John H. Zhang, Yun Peng Cao, Xue Jun Sun

Research output: Contribution to journalArticlepeer-review

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 languageEnglish
Pages (from-to)127-132
Number of pages6
JournalNeuroscience Letters
Volume491
Issue number2
DOIs
StatePublished - 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

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