Research Paper Volume 11, Issue 23 pp 11186—11201
Active compounds of herbs ameliorate impaired cognition in APP/PS1 mouse model of Alzheimer’s disease
- 1 Department of Neurology, The First Hospital of Hebei Medical University, Shijiazhuang, Hebei, China
- 2 Research Center, Hebei University of Chinese Medicine, Shijiazhuang, Hebei,China
- 3 Hebei Plant Bioreactor Preparation Technology Engineering Center, Shijiazhuang, Hebei, China
- 4 Hebei Chemical and Pharmaceutical College, Shijiazhuang, Hebei, China
Received: September 5, 2019 Accepted: November 18, 2019 Published: December 9, 2019
https://doi.org/10.18632/aging.102522How to Cite
Copyright © 2019 Yu et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Alzheimer’s disease (AD), the most common cause of dementia, is a neurodegenerative disorder characterized by amyloid plaque accumulations, intracellular tangles and neuronal loss in certain brain regions. It has been shown that a disturbance of normal iron metabolism contributes to the pathophysiology of AD. However, the mechanism underlying abnormal iron load in the brain of AD patients is unclear. The frontal cortex, an important brain structure for executive function, is one of the regions affected by AD. We investigated the beneficial effects of active compounds of Epimedium, Astragaoside and Puerarin on iron metabolism in the frontal cortex of six-month-old APPswe/PS1ΔE9 (APP/PS1) double transgenic mouse, a model of AD. Treatment with the active compounds reduced cognitive and memory deficits and damaged cell ultrastructure in APP/PS1 mice. These beneficial effects were associated with changes in expression levels of iron metabolism proteins in the frontal cortex, including divalent metal transporter with iron response element (DMT1-with IRE), divalent metal transporter without iron response element (DMT1-without IRE), transferrin (TF) and transferring receptor 1 (TfR1); three release proteins including the exporter ferroportin 1 (Fpn1), ceruloplasmin (CP) and hephaestin (HEPH), one increased storage iron protein ferritin and one iron regulating hormone hepcidin. These findings suggest that the active compounds improve cognition and memory in brain neurodegenerative disorders and these beneficial effects are associated with reduced impairment of iron metabolism. This study may provide a new strategy for developing novel drugs to treat AD.