Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2006-9-25
pubmed:abstractText
Prolonged or excessive exposure to corticosterone leads to neuronal damages in the brain regions, including hippocampus. We reported that astrocyte-conditioned medium (ACM) protected the neurons of the primary hippocampal cultures against the corticosterone-induced damages. Corticosterone added to the cultures resulted in a significant number of TUNEL-positive cells. However, corticosterone-induced TUNEL labeling was suppressed as for ACM-cultured neurons. To delineate the molecular basis underlying the neuroprotection of ACM, we assessed the activation of ERK1/2 and (PI3-K)/Akt signal pathways in response to corticosterone-induced neuronal damages. Western blot test revealed that corticosterone increased the phosphorylation of ERK1/2 and PI3-K/Akt in hippocampal neurons grown in Neurobasal medium supplemented with B27 and 500 microm L-glutamine (NBM+). Interestingly, the increase of phospho-ERK1/2 and Akt levels was much pronounced and the time course of phosphorylation was altered in ACM, suggesting that both signaling pathways might participate in ACM protection. Furthermore, the selective inhibitor of Akt, rather than ERK1/2, blocked the neuroprotective activity against corticosterone in ACM-cultured neurons. In summary, our data showed that ACM had a potent neuroprotective effect in cultured neurons. PI3-K/Akt signal pathway, but not ERK1/2, was involved in the protective activity against the corticosterone-induced damages.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
9
pubmed:volume
1114
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1-10
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:16930567-Analysis of Variance, pubmed-meshheading:16930567-Animals, pubmed-meshheading:16930567-Animals, Newborn, pubmed-meshheading:16930567-Astrocytes, pubmed-meshheading:16930567-Cells, Cultured, pubmed-meshheading:16930567-Corticosterone, pubmed-meshheading:16930567-Culture Media, Conditioned, pubmed-meshheading:16930567-Dose-Response Relationship, Drug, pubmed-meshheading:16930567-Drug Interactions, pubmed-meshheading:16930567-Embryo, Mammalian, pubmed-meshheading:16930567-Enzyme Activation, pubmed-meshheading:16930567-Enzyme Inhibitors, pubmed-meshheading:16930567-Female, pubmed-meshheading:16930567-Hippocampus, pubmed-meshheading:16930567-In Situ Nick-End Labeling, pubmed-meshheading:16930567-Mitogen-Activated Protein Kinase 3, pubmed-meshheading:16930567-Neurons, pubmed-meshheading:16930567-Phosphatidylinositol 3-Kinases, pubmed-meshheading:16930567-Pregnancy, pubmed-meshheading:16930567-Rats, pubmed-meshheading:16930567-Rats, Sprague-Dawley, pubmed-meshheading:16930567-Signal Transduction, pubmed-meshheading:16930567-Time Factors
pubmed:year
2006
pubmed:articleTitle
Astrocyte-conditioned medium protecting hippocampal neurons in primary cultures against corticosterone-induced damages via PI3-K/Akt signal pathway.
pubmed:affiliation
Department of Integrative Medicine and Neurobiology, Institute of Acupuncture Research, Shanghai Medical College, Fudan University, P.O. Box 291 138, Yi Xue Yuan Road, Shanghai 200032, PR China.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't