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

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

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DOI: 10.1016/j.neulet.2011.01.022 DOI is the universal ID for this study.

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This study is to examine if hydrogen-rich saline reduced amyloid-beta (A beta) induced neural inflammation and oxidative stress in a rat model by attenuation of activation of JNK and NF-kappa B. Sprague-Dawley male rats (n = 18,280-330 g) were divided into three groups, sham operated, A beta 1-42 injected and A beta 1-42 plus hydrogen-rich saline treated animals. Hydrogen-rich saline (5 ml/kg, i.p., daily) was injected for 10 days after intraventricular injection of A beta 1-42. The levels of IL-1 beta were assessed by ELISA analysis, 8-OH-dG by immunohistochemistry in the brain slides, and JNK and NF-kappa B by immunohistochemistry and western blotting. After A beta 1-42 injection, the level of IL-1 beta, 8-OH-dG, JNK and NF-kappa B all increased in brain tissues, while hydrogen-rich saline treatment decreased the level of IL-1 beta, 8-OH-dG and the activation of INK and NF-kappa B. In conclusion, hydrogen-rich saline prevented A beta-induced neuroinflammation and oxidative stress, possibly by attenuatation of activation of c-Jun NH(2)-terminal kinase (JNK) and nuclear factor-kappa B (NF-kappa B) in this rat model. (C) 2011 Elsevier Ireland Ltd. All rights reserved.

Publish Year 2011
Country China
Rank Positive
Journal Neuroscience Letters
Primary Topic Brain
Secondary TopicAlzheimer's Disease
Model Rat
Tertiary TopicAmyloid Beta Toxicity
Vehicle Saline (Dissolved)
pH Neutral
Application Injection