Linked Life Data

20599477

Source:http://linkedlifedata.com/resource/pubmed/id/20599477

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2010-8-9
pubmed:abstractText
Hypoxia which is mainly mediated by hypoxia-inducible factor 1 (HIF-1), can greatly contribute to the occurrence of Alzheimer's disease (AD) by increasing beta-site APP cleaving enzyme (BACE1) gene expression, protein level and beta-secretase activity, resulting in a significant generation of amyloid-beta (Abeta). Salidroside has been reported to have great neuroprotective effects. The aim of this study was to investigate the effects of salidroside on hypoxia-induced abnormal processing of the amyloid precursor protein (APP) in SH-SY5Y cells and its possible mechanism. Western blot analysis showed that 200muM of salidroside pretreatment significantly decreased BACE1 protein level and promoted the secretion of sAPPalpha in hypoxic condition. Salidroside had no effect on the level of APP, ADAM10 and ADAM17. ELISA analysis revealed that salidroside was able to inhibit the increase of beta-secretase activity and Abeta generation induced by hypoxia, with no effect on gamma-secretase activity. Notably, under hypoxia condition, mRNA of BACE1 and protein level of HIF-1alpha were decreased by salidroside pretreatment. These results demonstrated for the first time that salidroside was able to attenuate abnormal processing of amyloid precursor protein induced by hypoxia in SH-SY5Y cells, providing a new insight into prevention and treatment of Alzheimer's disease.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1872-7972
pubmed:author
pubmed:copyrightInfo
Copyright 2010 Elsevier Ireland Ltd. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
13
pubmed:volume
481
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
154-8
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Salidroside attenuates hypoxia-induced abnormal processing of amyloid precursor protein by decreasing BACE1 expression in SH-SY5Y cells.
pubmed:affiliation
Lab of Neurodegenerative Diseases and Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences(SIBS), Chinese Academy of Sciences(CAS), and Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't