4.7 Article

Ginsenosides attenuate D-galactose- and AlCl3-inducedspatial memory impairment by restoring the dysfunction of the neurotransmitter systems in the rat model of Alzheimer's disease

期刊

JOURNAL OF ETHNOPHARMACOLOGY
卷 194, 期 -, 页码 188-195

出版社

ELSEVIER IRELAND LTD
DOI: 10.1016/j.jep.2016.09.007

关键词

Ginsenosides; Alzheimer's disease; Morris water maze; Neurotransmitters; Liquid chromatography-mass spectrometry

资金

  1. National Natural Science Foundation of China [21505048, 81530094]

向作者/读者索取更多资源

Ethnopharmacological relevance: Panax ginseng C.A.Mey. is a traditional Chinese herbal medicine, which has been used to treat Alzheimer's disease (AD) for thousands of years. Ginsenoside is one of the major compounds found in P. ginseng. This study aimed to explore the attenuation of spatial memory impairment by ginsenosides and its correlation with restoring the dysfunction of the neurotransmitter systems in AD model rats to understand the mechanism underlying the anti-AD effect of R ginseng. Materials and methods: In this study, the AD model was established by combining D-galactose (D-gal) with AlCl3 (Al) for 60 days. From day 30, the ginsenosides group was intragastrically administered with ginsenosides for 30 days. The ethology of rats was tested through the Morris water maze test(MWM). Histopathological changes in the hippocampus of rats were observed through hematoxylin and eosin staining. The expressions of amyloid beta peptide (A beta) and phospho-tau (p-tau) in the hippocampus and cortex of rats were detected by immunohistochemistry. A liquid chromatography mass spectrometry assay was used to measure neurotransmitter concentrations in the hippocampus, cortex, and blood. Results: Ginsenosides could significantly decrease the escape latency time and the average latency time in the place navigation test and increase the times of crossing the platform area, the percentage of residence time, and the distance in the original platform quadrant in the spatial probe test Ginsenosides could repair the damage of the hippocampus and reduce the expressions of A beta and p-tau. Ginsenosides could also increase gamma-aminobutyric acid, acetylcholine, and dopamine levels and decrease glutamate and aspartic acid levels in the hippocampus and cortex and increase glycine and serotonin levels in the blood. Conclusions: After effectively administrated, ginsenosides attenuate D-gal- and Al-induced spatial memory impairment. The possible mechanism of the beneficial effect is restoring the dysfunction of various neurotransmitters. (C) 2016 Elsevier Ireland Ltd. All rights reserved.

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