4.7 Article

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

期刊

JOURNAL OF ETHNOPHARMACOLOGY
卷 179, 期 -, 页码 162-169

出版社

ELSEVIER IRELAND LTD
DOI: 10.1016/j.jep.2015.12.020

关键词

Alzheimer's disease; Ginseng; Neuroprotective; Protein

资金

  1. Ph. D. Programs Foundation of Ministry of Education of China [2013M530945]
  2. Liaoning Science and Technology Department [2008226011-1]
  3. National Natural Science Foundation of China [81173580, 81210108050]

向作者/读者索取更多资源

Ethnopharmacological relevance: Alzheimer 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 methods: The AD rat model was established by intraperitoneally injecting D-galactose [60 mg/(kg d)] followed by intragastrically administering AlCl3 [40 mg/(kg d)] for 90 days. From day 60, the GP groups were intragastrically administered with GP 0.05 or 0.1 g/kg twice daily for 30 days. The ethology of rats was tested by Morris water maze test. The content of A beta(1-42) and p-tau in the hippo campus of rats was detected by enzyme-linked immunosorbent assay. The expression of mRNA5 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. Results: GP 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 A beta(1-42) and p-tau and improved the mRNA and protein expression of PI3K, p-Akt/Akt, and Bcl-2/Bax in die hippocampus. Conclusions: GP could improve the memory ability and reduce the content of A beta(1-42) and p-tau in AD rats. The anti-AD effects of GP were in part mediated by PI3K/Akt signaling pathway activation. (C) 2015 Elsevier Ireland Ltd. All rights reserved.

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