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

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 NH2-terminal kinase (JNK) and nuclear factor-kappa B (NF-kappa B) in this rat model. (C) 2011 Elsevier Ireland Ltd. All rights reserved.