Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2010-8-9
pubmed:abstractText
N-stearoyltyrosine (NsTyr), an anandamide (AEA) analogue is similar to AEA not only structurally but also in terms of biological activity. Since A beta-induced neuronal injury triggers the activation of mitogen-activated protein kinase (MAPK) pathways and the induction or activation of pro- and anti-apoptotic proteins, in the present study we aimed to assess the protective effect of NsTyr against A beta induced neuronal apoptosis. Cell viability and neuronal injury were respectively measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay and lactate dehydrogenase (LDH) assay. Hoechst staining and flow cytometric assessment were used to evaluate cell apoptosis. The anti-apoptotic mechanism involved MAPK phosphorylation and Bcl-2/Bax expression was investigated. The best neuroprotective effect on A beta 25-35-induced neuronal apoptosis was observed in the presence of NsTyr (1 microM). NsTyr exerted anti-apoptotic effect at least partly via activating p-ERK-Bcl-2 but suppressing p-p38-Bax pathways. Moreover a dynamic balance between p-ERK and p-p38 MAPK pathways in NsTyr-induced neuronal protection suggested an interaction between them. Our results indicated the neuroprotective effect of NsTyr on A beta 25-35-induced neuronal injury was at least partly due to anti-apoptosis and raised the possibility that NsTyr might reduce neurodegenerative disorders.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1873-7544
pubmed:author
pubmed:copyrightInfo
(c) 2010 IBRO. Published by Elsevier Ltd. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
169
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1840-7
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
N-stearoyltyrosine protects primary neurons from A?-induced apoptosis through modulating mitogen-activated protein kinase activity.
pubmed:affiliation
Department of Pharmacy, Institute of Medical Sciences, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, PR China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't