Linked Life Data

15663961

Source:http://linkedlifedata.com/resource/pubmed/id/15663961

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2005-1-24
pubmed:abstractText
Cytokine interleukin-6 (IL-6) has been showed to be an important mediator of neuroimmune responses. However, effects of IL-6 in the central nervous system (CNS) are quite complex and diverse, and mechanisms through which IL-6 influences neuronal functions are primarily unknown. In the present study, we explored protective effect of IL-6 that was chronically applied to cerebellar granule neurons (CGNs) in culture against neurodamage induced by glutamate and mechanisms involved in the neuroprotective effect of IL-6. The chronic IL-6 exposure significantly prevented the CGNs from the glutamate-induced attenuation of neuronal vitality. This neuroprotective effect of IL-6 depended on its concentrations. IL-6 at 2.5 ng/ml did not markedly improve the neuronal vitality, but IL-6 at 5 and 10 ng/ml notably improved the neuronal vitality. The glutamate-evoked neuronal apoptosis also was strikingly inhibited by the chronic IL-6 pretreatment. Intracellular Ca2+ in the CGNs lacking IL-6 pretreatment acutely rose as soon as these neurons were stimulated by glutamate and were maintained at higher levels during the whole 18-min period of glutamate attack. Although intracellular Ca2+ in the IL-6-pretreated CGNs also produced an acute and transient elevation in response to the glutamate insult, they quickly dropped and recovered to basal levels before the glutamate application. Anti-gp130 monoclonal antibody (mAb) blocked the suppressive effect of IL-6 on the glutamate-induced intracellular Ca2+ overload. These results reveal that IL-6 can protect neurons against glutamate-induced neurotoxicity, and suggest that the neuroprotective effect of IL-6 may be via gp130 signal transducing pathway to suppress the glutamate-evoked intracellular Ca2+ overload.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0304-3940
pubmed:author
pubmed:issnType
Print
pubmed:day
21
pubmed:volume
374
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
192-6
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:15663961-Animals, pubmed-meshheading:15663961-Animals, Newborn, pubmed-meshheading:15663961-Antibodies, Monoclonal, pubmed-meshheading:15663961-Antigens, CD, pubmed-meshheading:15663961-Calcium, pubmed-meshheading:15663961-Cell Count, pubmed-meshheading:15663961-Cell Death, pubmed-meshheading:15663961-Cell Survival, pubmed-meshheading:15663961-Cells, Cultured, pubmed-meshheading:15663961-Cerebellum, pubmed-meshheading:15663961-Cytokine Receptor gp130, pubmed-meshheading:15663961-Dose-Response Relationship, Drug, pubmed-meshheading:15663961-Drug Interactions, pubmed-meshheading:15663961-Glutamic Acid, pubmed-meshheading:15663961-In Situ Nick-End Labeling, pubmed-meshheading:15663961-Interleukin-6, pubmed-meshheading:15663961-Membrane Glycoproteins, pubmed-meshheading:15663961-Neurons, pubmed-meshheading:15663961-Rats, pubmed-meshheading:15663961-Rats, Sprague-Dawley
pubmed:year
2005
pubmed:articleTitle
Interleukin-6 protects cultured cerebellar granule neurons against glutamate-induced neurotoxicity.
pubmed:affiliation
Department of Biological Science and Technology and State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Mailbox 426, Nanjing University, 22 Hankou Road, Nanjing 210093, China.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't