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dc.contributor.authorWang, Yuhui
dc.contributor.authorShen, Jinyang
dc.contributor.authorYang, Xiaolin
dc.contributor.authorJin, Ye
dc.contributor.authorYang, Zhonglin
dc.contributor.authorWang, Rufeng
dc.contributor.authorZhang, Fuming
dc.contributor.authorLinhardt, Robert J.
dc.identifier.citationAkebia 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.
dc.descriptionBiomedical Pharmacotherapy 107, 219-225
dc.descriptionNote : 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.
dc.description.abstractBackground: 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.
dc.description.sponsorshipNational Natural Science Foundation of China
dc.relation.ispartofThe Linhardt Research Labs Online Collection
dc.relation.ispartofRensselaer Polytechnic Institute, Troy, NY
dc.relation.ispartofBiomedicine and Pharmacotherapy
dc.subjectChemistry and chemical biology
dc.subjectChemical and biological engineering
dc.subjectBiomedical engineering
dc.titleAkebia saponin D reverses corticosterone hypersecretion in an Alzheimer's disease rat model
dc.rights.holderIn Copyright : this Item is protected by copyright and/or related rights. You are free to use this Item in any way that is permitted by the copyright and related rights legislation that applies to your use. For other uses you need to obtain permission from the rights-holder(s).
dc.relation.departmentThe Linhardt Research Labs.
dc.relation.departmentThe Shirley Ann Jackson, Ph.D. Center for Biotechnology and Interdisciplinary Studies (CBIS)

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