Effect of Fermented Red Ginseng on Memory Impairment and β-amyloid Reduction in Alzheimer's Disease Experimental Models
- Effect of Fermented Red Ginseng on Memory Impairment and β-amyloid Reduction in Alzheimer's Disease Experimental Models
- 김준기; 김성훈; Lee Deuk-Sik; Lee Dong-Jin; Kim Soo-Hyun; Chung Sungkwon; 양현옥
- Alzheimer's Disease; Fermented Red Ginseng; Memory; Beta-Amyloid
- Issue Date
- 2012 International Congress of Korean Federation of Pharmaceutical Societies
- This study examined the effect of fermented red ginseng (FRG) on memory impairment and β-amyloid reduction in Alzheimer’s disease (AD) in vitro and in vivo experimental models. FRG extract was manufactured through steaming, drying and fermentation with Lactobacillus fermentum. For the comparison, heat-dried ginseng (DG) extract was used. The effect of FRG and DG extracts on in vitro soluble Aβ42 level was conducted by incubating HeLa cell line stably expressing Swedish mutant form of APP (APPswe) with extracts. After 8 h of incubation, soluble Aβ42 level was attenuated to 70% with FRG treatment whereas DG extract exhibited no difference from control group. To find out the effect of FRG extract on in vivo memory impairment, scopolamine injected ICR mice were tested for passive avoidance. FRG treatment exhibited significant elevation of entry latency during test session. Memory enhancing effect was confirmed with transgenic (TG) mice model of AD. TG mice were orally treated with FRG extract 400 and 800 mg/kg for 4 months starting at the age of 7 months old. Morris water maze test was conducted to find out the effect of FRG extract on spatial memory function of the mice. FRG treated groups showed significant dose-dependent decrease of escape latency during acquisition phase, and tendency of increased duration in target quadrant was observed during retention phase compared to TG control group. Brain soluble Aβ42 level was also measured from the cerebral cortex of TG mice. The soluble Aβ42 level was significantly elevated in TG mice. This elevation was significantly reduced by treatment of FRG extract. These findings suggest that FRG extract protects brain from increase of Aβ42 level, resulting enhanced behavioral memory function which can be applied for prevention or treatment of AD.
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