Neuroprotective effects of ginseng protein on PI3K/Akt signaling pathway in the hippocampus of D-galactose/AlCl3 inducing rats model of Alzheimer’s disease

Publication date: 17 February 2016
Source:Journal of Ethnopharmacology, Volume 179
Author(s): Hongyan Li, Tingguo Kang, Bin Qi, Liang Kong, Yanan Jiao, Yang Cao, Jianghua Zhang, Jingxian Yang
Ethnopharmacological relevanceAlzheimer disease (AD) is a progressive neurodegenerative disease, with progressive memory loss, cognitive deterioration, and behavioral disorders. Ginseng (Panax ginseng C.A. Meyer) is widely used in China to treat various kinds of nervous system disorders. The study aimed to explore the therapeutic effect of ginseng protein (GP) on Alzheimer's disease and its correlation with the PI3K/Akt signaling pathway to understand the mechanism underlying the neuroprotective effect of ginseng.Material and methodsThe AD rat model was established by intraperitoneally injecting D-galactose [60mg/(kgd)] followed by intragastrically administering AlCl3 [40mg/(kgd)] for 90 days. From day 60, the GP groups were intragastrically administered with GP 0.05 or 0.1g/kg twice daily for 30 days. The ethology of rats was tested by Morris water maze test. The content of Aβ1-42 and p-tau in the hippocampus of rats was detected by enzyme-linked immunosorbent assay. The expression of mRNAs and proteins of PI3K, Akt, phosphorylated Akt (p-Akt), Bcl-2, and Bax in the hippocampus was detected by real-time quantitative reverse transcription polymerase chain reaction and Western blot assay.ResultsGP was found to significantly improve the memory ability of AD rats and prolong the times of crossing the platform and the percentage of residence time in the original platform quadrant of spatial probe test. GP also reduced the content of Aβ1-42 and p-tau and improved the mRNA and protein expression of PI3K, p-Akt/Akt, and Bcl-2/Bax in the hippocampus.ConclusionsGP could improve the memory ability and reduce the content of Aβ1-42 and p-tau in AD rats. The anti-AD effects of GP were in part mediated by PI3K/Akt signaling pathway activation.

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