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. (24th December 2016)

• Record Type: Journal Article
• Authors: Zhang, Yan; Pi, Zifeng; Song, Fengrui; Liu, Zhiqiang
• Is Part Of: Journal of ethnopharmacology. Volume 194(2016)
• Page Start: 188
• Page End: 195
• Publication Date: 2016-12-24
• Subjects: D-Galactose (PubChem CID: 6036) -- Glutamate (PubChem CID: 33032) -- Aspartic acid(PubChem CID: 424) -- γ-aminobutyric acid (PubChem CID: 119) -- Glycine (PubChem CID: 750) -- Dopamine (PubChem CID: 65340) -- Serotonin (PubChem CID: 5202) -- Acetylcholine (PubChem CID: 187) -- AlCl3 (PubChem CID: 24012); Ginsenosides -- Alzheimer's disease -- Morris water maze -- Neurotransmitters -- Liquid chromatography–mass spectrometry; Ethnopharmacology -- Periodicals; Pharmacognosy -- Periodicals; Herbs -- Periodicals; Herbs -- Periodicals; Pharmacognosy -- Periodicals; Pharmacognosie -- Périodiques; Herbes -- Périodiques; 615.1
• DOI: 10.1016/j.jep.2016.09.007
• Languages: English
• ISSNs: 0378-8741

Abstract

Abstract: 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 P. ginseng . Materials and methods: In this study, the AD model was established by combiningd -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 β peptide (Aβ) 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 Aβ and p-tau. Ginsenosides could also increase γ-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 attenuated -gal- and Al-induced spatial memory impairment. The possible mechanism of the beneficial effect is restoring the dysfunction of various neurotransmitters. Graphical abstract: