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Molecules 2016, 21(3), 323; doi:10.3390/molecules21030323

Treatment with Akebia Saponin D Ameliorates Aβ1–42-Induced Memory Impairment and Neurotoxicity in Rats

1
Department of Pharmacology, China Pharmaceutical University, 24 Tongjia Xiang, Nanjing 210009, Jiangsu, China
2
College of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, Jiangsu, China
3
State Key Laboratory of Natural Medicines, Department of Physiology, China Pharmaceutical University, 24 Tongjia Xiang, Nanjing 210009, Jiangsu, China
*
Authors to whom correspondence should be addressed.
Academic Editors: Michael Decker and Diego Muñoz-Torrero
Received: 20 January 2016 / Revised: 1 March 2016 / Accepted: 2 March 2016 / Published: 8 March 2016
(This article belongs to the Special Issue Molecules against Alzheimer)
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Abstract

Amyloid-β peptide (Aβ) is known to be directly associated with the progressive neuronal death observed in Alzheimer’s disease (AD). However, effective neuroprotective approaches against Aβ neurotoxicity are still unavailable. In the present study, we investigated the protective effects of Akebia saponin D (ASD), a typical compound isolated from the rhizome of Dipsacus asper Wall, on Aβ1–42-induced impairment of learning and memory formation and explored the probable underlying molecular mechanisms. We found that treatment with ASD (30, 90 or 270 mg/kg) significantly ameliorated impaired spatial learning and memory in intracerebroventricularly (ICV) Aβ1–42-injected rats, as evidenced by a decrease tendency in escape latency during acquisition trials and improvement in exploratory activities in the probe trial in Morris water maze (MWM). Further study showed that ASD reversed Aβ1–42-induced accumulation of Aβ1–42 and Aβ1–40 in the hippocampus through down-regulating the expression of BACE and Presenilin 2 accompanied with increased the expression of TACE, IDE and LRP-1. Taken together, our findings suggested that ASD exerted therapeutic effects on Aβ-induced cognitive deficits via amyloidogenic pathway. View Full-Text
Keywords: Alzheimer’s disease; Akebia Saponin D (ASD); Amyloid β (Aβ)1–42; cognitive impairment; neurotoxicity Alzheimer’s disease; Akebia Saponin D (ASD); Amyloid β (Aβ)1–42; cognitive impairment; neurotoxicity
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Chen, Y.; Yang, X.; Chen, T.; Ji, J.; Lan, L.; Hu, R.; Ji, H. Treatment with Akebia Saponin D Ameliorates Aβ1–42-Induced Memory Impairment and Neurotoxicity in Rats. Molecules 2016, 21, 323.

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