Akebia saponin D reverses corticosterone hypersecretion in an Alzheimer's disease rat model
Authors
Wang, Yuhui
Shen, Jinyang
Yang, Xiaolin
Jin, Ye
Yang, Zhonglin
Wang, Rufeng
Zhang, Fuming
Linhardt, Robert J.
ORCID
https://orcid.org/0000-0003-2219-5833
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Other Contributors
Issue Date
2018-11-01
Keywords
Biology , Chemistry and chemical biology , Chemical and biological engineering , Biomedical engineering
Degree
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Full Citation
Akebia saponin D reverses corticosterone hypersecretion in an Alzheimer's disease rat model. Y. Wang, J. Shen, X. Yang, Y. Jin, Z. Yang, R. Wang, F. Zhang, R.J. Linhardt, Biomedical Pharmacotherapy 107, 219-225, 2018.
Abstract
Background: Glucocorticoid hormones are implicated in the pathogenesis of Alzheimer's disease (AD) and other diseases including diabetes, hyperlipidemia, and osteoporosis. Akebia saponin D (ASD) possesses numerous pharmacological activities, including as an anti-AD, anti-hyperlipidemia, anti-diabetes, and anti-osteoporosis agent. The anti-AD effect of ASD is possibly through its regulation of glucocorticoid levels. Purpose: The present study was undertaken to investigate the neuroprotective effects of ASD on Aβ25-35-induced cognitive deficits and to elucidate its underlying mechanism of action. Methods: The AD rat model was established by an intracerebroventricular injection of Aβ25-35 into the lateral ventricles. Spatial learning and anxiety state were assessed by Morris water maze task and elevated plus-maze assay, respectively. The degree of hypertrophy of adrenal gland was analyzed using the viscera coefficient. Corticosterone and ACTH concentrations in the plasm were measured using biochemical assay kits. The activity of 11β-hydroxysteroid dehydrogenase type-1 (11β-HSD1) in liver and groin fat pad was assessed by measuring cortisol production. Results: Compared with the control group, AD rats displayed significant spatial learning and reference memory impairments, serious anxiety disorders, obvious hypertrophy of adrenal gland, elevated corticosterone and ACTH levels in the plasma, and increased 11β-HSD1 activity in liver and groin fat pad. ASD could significantly ameliorate the memory deficits and anxiety symptoms, markedly reduce the viscera coefficient of adrenal gland, observably decrease corticosterone and ACTH concentrations, and showed no effect on the activity of 11β-HSD1. Conclusions: These results indicate that ASD might exert a significant neuroprotective effect on cognitive impairment, driven in part by reducing systemic corticosterone level by down-regulation of the hypothalamic-pituitary-adrenal (HPA) axis.
Description
Biomedical Pharmacotherapy 107, 219-225
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Note : if this item contains full text it may be a preprint, author manuscript, or a Gold OA copy that permits redistribution with a license such as CC BY. The final version is available through the publisher’s platform.
Department
The Linhardt Research Labs.
The Shirley Ann Jackson, Ph.D. Center for Biotechnology and Interdisciplinary Studies (CBIS)
The Shirley Ann Jackson, Ph.D. Center for Biotechnology and Interdisciplinary Studies (CBIS)
Publisher
Relationships
The Linhardt Research Labs Online Collection
Rensselaer Polytechnic Institute, Troy, NY
Biomedicine and Pharmacotherapy
https://harc.rpi.edu/
Rensselaer Polytechnic Institute, Troy, NY
Biomedicine and Pharmacotherapy
https://harc.rpi.edu/
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https://login.libproxy.rpi.edu/login?url=https://doi.org/10.1016/j.biopha.2018.07.149