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Akebia Saponin D attenuates amyloid beta-induced cognitive deficits and inflammatory response in rats: involvement of Akt/NF-kappaB pathway.

Authors: Yu, X  Wang, LN  Du, QM  Ma, L  Chen, L  You, R  Liu, L  Ling, JJ  Yang, ZL  Ji, H 
Citation: Yu X, etal., Behav Brain Res. 2012 Dec 1;235(2):200-9. doi: 10.1016/j.bbr.2012.07.045. Epub 2012 Aug 8.
Pubmed: (View Article at PubMed) PMID:22963993
DOI: Full-text: DOI:10.1016/j.bbr.2012.07.045

Neuroinflammatory responses caused by amyloid beta(Abeta) play an important role in the pathogenesis of Alzheimer's disease (AD). Abeta is known to be directly responsible for the activation of glial cells and induction of apoptosis. Akebia Saponin D (ASD) is extracted from a traditional herbal medicine Dipsacus asper Wall, which has been shown to protect against ibotenic acid-induced cognitive deficits and cell death in rats. In this study, we investigated the in vivo protective effect of ASD on learning and memory impairment induced by bilateral intracerebroventricular injections of Abeta1-42 using Morris water and Y-maze task. Furthermore, the anti-inflammatory activity and neuroprotective effect of ASD was examined with methods of histochemistry and biochemistry. These data showed that oral gavage with ASD at doses of 30, 90 and 270 mg/kg for 4 weeks exerted an improved effect on cognitive impairment. Subsequently, the ASD inhibited the activation of glial cells and the expression of tumor necrosis factor (TNF)-alpha, interleukin-1 beta (IL-1beta) and cyclooxygenase-2 (COX-2) in rat brain. Moreover, ASD afforded beneficial actions on inhibitions of Akt and IkappaB kinase (IKK) phosphorylations, as well as nuclear factor kappaB (NF-kappaB) activation induced by Abeta1-42. These results suggest that ASD may be a potential agent for suppressing both Alzheimer's disease-related neuroinflammation and memory system dysfunction.


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CRRD Object Information
CRRD ID: 7204700
Created: 2012-12-27
Species: All species
Last Modified: 2012-12-27
Status: ACTIVE


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