Hydrogen-rich saline improves memory function in a rat model of amyloid-beta-induced Alzheimer's disease by reduction of oxidative stress

莫里斯水上航行任务 氧化应激 神经炎症 海马体 生理盐水 β淀粉样蛋白 胶质纤维酸性蛋白 化学 内分泌学 内科学 淀粉样蛋白(真菌学) 炎症 医学 免疫组织化学 病理 疾病
作者
Jian Li,Cai Wang,John H. Zhang,Jianmei Cai,Yunpeng Cao,Xuejun Sun
出处
期刊:Brain Research [Elsevier]
卷期号:1328: 152-161 被引量:194
标识
DOI:10.1016/j.brainres.2010.02.046
摘要

This study is to examine if hydrogen-rich saline reduced amyloid β (Aβ) induced neural inflammation, and learning and memory deficits in a rat model. S-D male rats (n = 84, 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 14 days after intracerebroventricular injection of Aβ1-42. The levels of MDA, IL-6 and TNF-α were assessed by biochemical and ELISA analysis. Morris Water Maze and open field task were used to assess the memory dysfunction and motor dysfunction, respectively. LTP were used to detect the electrophysiology changes, HNE and GFAP immunohistochemistry were used to assess the oxidative stress and glial cell activation. After Aβ1-42 injection, the levels of MDA, IL-6, and TNF-α were increased in brain tissues and hydrogen-rich saline treatment suppressed MDA, IL-6, and TNF-α concentration. Hydrogen-rich saline treatment improved Morris Water Maze and enhanced LTP in hippocampus blocked by Aβ1-42. Furthermore, hydrogen-rich saline treatment also decreased the immunoreactivitiy of HNE and GFAP in hippocampus induced by Aβ1-42. In conclusion, hydrogen-rich saline prevented Aβ-induced neuroinflammation and oxidative stress, which may contribute to the improvement of memory dysfunction in this rat model.

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