• QianKun Quan, Jue Wang, Xi Li, and Yi Wang.
• The Key Laboratory of Biomedical Information Engineering of Ministry of Education, and Institute of Biomedical Engineering, School of Life Science and Technology, Xi'an Jiaotong University, National Engineering Research Center of Health Care and Medical Devices, Xi'an, China.
• Plos One. 2013 Jan 1;8(3):e59155.

Background And PurposeThe present study was designed to examine the effects of ginsenoside Rg1 on expression of peroxisome proliferator-activated receptor γ (PPARγ) and insulin-degrading enzyme (IDE) in the hippocampus of rat model of Alzheimer's disease (AD) to determine how ginsenoside Rg1 (Rg1) decreases Aβ levels in AD.Experimental ApproachExperimental AD was induced in rats by a bilateral injection of 10 µg soluble beta-amyloid peptide 1-42 (Aβ(1-42)) into the CA1 region of the hippocampus, and the rats were treated with Rg1 (10 mg·kg(-1), intraperitoneally) for 28 days. The Morris water maze was used to test spatial learning and memory performance. Hematoxylin-eosin staining was performed to analyze the hippocampal histopathological damage. Immunohistochemistry, western blotting, and real-time PCR were used to detect Aβ(1-42), PPARγ, and insulin-degrading enzyme (IDE) expression in the hippocampus.Key ResultsInjection of soluble Aβ(1-42) into the hippocampus led to significant dysfunction of learning and memory, hippocampal histopathological abnormalities and increased Aβ(1-42) levels in the hippocampus. Rg1 treatment significantly improved learning and memory function, attenuated hippocampal histopathological abnormalities, reduced Aβ(1-42) levels and increased PPARγ and IDE expression in the hippocampus; these effects of Rg1 could be effectively inhibited by GW9662, a PPARγ antagonist.Conclusions And ImplicationsGiven that PPARγ can upregulate IDE expression and IDE can degrade Aβ(1-42), these results indicate that Rg1 can increase IDE expression in the hippocampus by upregulating PPARγ, leading to decreased Aβ levels, attenuated hippocampal histopathological abnormalities and improved learning and memory in a rat model of AD.

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