Hydrogen-rich saline demonstrated neuroprotective effects in an amyloid-beta-induced Alzheimer's disease rat model by reducing neuroinflammation and oxidative stress markers through inhibition of JNK and NF-kappa B signaling pathways. The treatment decreased pro-inflammatory cytokine IL-1 beta and oxidative damage marker 8-OH-dG in brain tissue. However, this study has been retracted and should not be considered reliable evidence for clinical application.
Plain-Language Summary
This study, which has been retracted and is no longer considered reliable, tested whether hydrogen-rich saline could reduce brain damage in rats given a substance that mimics Alzheimer's disease. Researchers found that the hydrogen-rich saline appeared to decrease markers of inflammation and oxidative stress (cellular damage from unstable molecules) in rat brains, possibly by blocking certain signaling pathways. However, because this paper was retracted, its findings should not be relied upon.
Abstract
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.
