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 (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, 280–330 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 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.

Research highlights
► Hydrogen-rich saline can reduce the hydroxyl radicals in the rat model of AD.
► Hydrogen-rich saline have anti-inflammation effect in the rat model of AD.
► Hydrogen-rich saline impede activation of JNK and NF-κB induced by Aβ1–42 in the rat model.