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.
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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