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Original Research Article | OPEN ACCESS

Epimedium brevicornu Maxim extract shows protective activity against Alzheimer disease in mice

Jiang-hua Xu1, Mei Li1, Guang-sheng Wang2, Zi-ran Zhao1

1Department of Neurology, Yantai Yeda Hospital, Yantai 264000; 2Department of Neurology, Jinan Sixth People's Hospital, Jinan 250200, Shandong Province, China.

For correspondence:-  Zi-ran Zhao   Email: zhaoziran133@126.com   Tel:+8617705358825

Accepted: 24 July 2019        Published: 29 August 2019

Citation: Xu J, Li M, Wang G, Zhao Z. Epimedium brevicornu Maxim extract shows protective activity against Alzheimer disease in mice. Trop J Pharm Res 2019; 18(8):1739-1743 doi: 10.4314/tjpr.v18i8.25

© 2019 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To investigate the protective effect of Epimedium brevicornu Maxim extract (EBME) against Alzheimer's disease in 3xTg-AD mice.
Methods: The cognitive function of 3xTg-AD mice was assessed using Morris water maze test. The levels of amyloid beta deposits and NeuN in the mouse hippocampus were evaluated by immunohistochemistry. Brain neurotrophic-derived factor (BDNF) and tyrosine kinase B (TrkB) expressions were examined by western blot analysis.
Results: EBME treatment significantly ameliorated learning and memory deficits in AD mice, as shown by the increased time spent in the target zone during probe tests. Compared with the 3xTg-AD mice (8.4 ± 1.1 s), the escape latency in animals treated with 600 mg/kg EBME (21.5 ± 1.1 s) was significantly increased (p < 0.01). In addition, EBME significantly decreased Aβ deposits, increased NeuN-positive cells, and upregulated the expressions of BDNF (1.5 ± 0.2, p < 0.05) and TrkB (1.6 ± 0.2, p < 0.05) in the 3xTg AD mice.
Conclusion:  EBME treatment may be a useful therapeutic strategy for managing memory impairment.

Keywords: Epimedium brevicornu, Alzheimer's disease, Memory impairment, NeuN-positive cells, Amyloid beta deposits

Impact Factor
Thompson Reuters (ISI): 0.523 (2021)
H-5 index (Google Scholar): 39 (2021)

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