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Original Research Article | OPEN ACCESS

Protective effect of Acorus tatarinowii extract against alzheimer in 3xTg-AD mice

Cen Su1, Ping Niu2 , Yao-ming Xu3, Ye Feng2, Hai-ping Xia1

1Department of Neurology, the Fourth Hospital of Jiangsu University, Zhenjiang 212001; 2Department of Neurology, the General Hospital of Shenyang Military, Shenyang110004; 3Department of Neurology, Tongliao Hospital of Inner Mongolia Autonomous Region, Tongliao 028000, China.

For correspondence:-  Ping Niu   Email: niuping494@126.com   Tel:+8651184425614

Accepted: 23 August 2019        Published: 01 October 2019

Citation: Su C, Niu P, Xu Y, Feng Y, Xia H. Protective effect of Acorus tatarinowii extract against alzheimer in 3xTg-AD mice. Trop J Pharm Res 2019; 18(9):1903-1907 doi: 10.4314/tjpr.v18i9.17

© 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 Acorus tatarinowii extract (ATE) against Alzheimer's disease in 3xTg-AD mice.
Method: The cognitive function of 3xTg-AD mice was assessed using Morris water maze test. The levels of the amyloid beta deposits and NeuN in the hippocampus were evaluated by immunohistochemical assay while brain neurotrophic derived factor (BDNF) and tyrosine kinase B (TrkB) expressions were determined by western blot analysis.
Results: ATE treatment significantly ameliorated learning and memory deficits in AD mice, as shown by increased time spent in the target zone during probe tests. The escape latency in animals treated with 600 mg/kg ATE (24.8 ± 1.3 s) was significantly increased relative to ontreated 3xTg-AD mice (8.5 ± 1.0 s, p < 0.01). In addition, ATE significantly decreased Aβ deposits, increased NeuN-positive cells, and upregulated the expression of BDNF (1.9 ± 0.4, p < 0.05) and TrkB (1.9 ± 0.2, p < 0.05) in 3xTg AD mice.
Conclusion: These results suggest that ATE treatment may be a useful strategy for managing memory impairment induced by several neurodegenerative diseases.

Keywords: Acorus tatarinowii, Alzheimer's disease, Neurodegenerative diseases, 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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