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Hydrogen-rich Saline Improves Memory Function in a Rat Model of Amyloid-beta-induced Alzheimer’s Disease by Reduction of Oxidative Stress

 

 

aDepartment of Neurology, the first affiliated hospital of China Medical University, Shengyang 110001, China; bDepartment of Neurosurgery, Loma Linda University, California, CA, USA; cDepartment of Diving Medicine, Faculty of Naval Medicine, Second Military Medical University, Shanghai, PR China

 

Corresponding authors: Yun-peng CAO, Department of neurology, First afflicted Hospital, China Medical University, Shenyang, 110001, PR China.

Telephone: (86)2483282516, Fax: (86)2483282385. E-mail: ypengcao@yahoo.com;

Xue-jun Sun, Department of Diving Medicine, Faculty of Naval Medicine, Second Military Medical University, Shanghai, 200433, PR China. Tel: (86)2125070349. Fax: (86)2165492382. Email: sunxjk@hotmail.com

 


Abstract

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, 280-330g) 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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