Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2008-3-21
pubmed:abstractText
l-3-n-Butylphthalide (l-NBP), as an anti-cerebral ischemia agent, has been shown to have therapeutic effects on learning and memory deficits induced by chronic cerebral hypoperfusion and Abeta intracerebroventricular infusion in rats. In the present study, we investigated the neuroprotective effects of l-NBP on beta-amyloid (Abeta)25-35-induced neuronal death/apoptosis and potential mechanisms in rat hippocampal neurons and human neuroblastoma SH-SY5Y cells. Abeta25-35 significantly reduced cell viability and increased the number of apoptotic-like cells, indicating that Abeta25-35-induced neurotoxicity. In addition, tau protein hyperphosphorylation was found to increase after Abeta exposure. All of these phenotypes induced by Abeta25-35 were markedly reversed by l-NBP. Pretreatment with l-NBP prior to Abeta25-35 exposure significantly elevated cell viability, and reduced Abeta25-35-induced nuclear fragmentation and early apoptosis. Furthermore, immunoreactivity for hyperphosphorylation tau protein was significantly decreased by l-NBP treatment. Our results suggest that l-NBP may protect neurons against Abeta-induced neurotoxicity via inhibiting tau protein hyperphosphorylation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0304-3940
pubmed:author
pubmed:issnType
Print
pubmed:day
28
pubmed:volume
434
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
224-9
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
l-3-n-Butylphthalide ameliorates beta-amyloid-induced neuronal toxicity in cultured neuronal cells.
pubmed:affiliation
Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, No. 1, Xiannongtan Street, Xuanwu District, Beijing 100050, China.
pubmed:publicationType
Journal Article