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Mitogen-activated protein kinases activated by lipopolysaccharide and beta-amyloid in cultured rat microglia.

Authors
Pyo, H; Jou, I; Jung, S; Hong, S; Joe, EH
Citation
Neuroreport, 9(5):871-874, 1998
Journal Title
Neuroreport
ISSN
0959-49651473-558X
Abstract
To test whether mitogen-activated protein kinases (MAPKs) are involved in microglial activation, pure microglia prepared from 1- to 3-day-old rat brains were activated with either 100 ng/ml lipopolysaccharide (LPS) or 5 nM synthetic beta-amyloid (Abeta) (25-35). The patterns of MAPK activation following LPS and Abeta treatment were very similar. Three MAPK subtypes, p38, extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) were activated within 15 min and the activities of p38 and ERK were rapidly reduced to background level within 30 min while that of JNK was maintained for over 1 h. Both inhibitors of p38 (SB203580) and ERK pathway (PD098059) reduced LPS-induced nitric oxide (NO) release and Abeta-induced tumor necrosis factor-alpha (TNF-alpha) release. Furthermore, co-treatment of SB203580 and PD098059 additively reduced NO and TNF-alpha release. These results suggest that MAPK, at least p38 and ERK, mediate LPS-, and Abeta-induced microglial activation.
MeSH terms
Amyloid beta-Peptides/*pharmacologyAnimalsCalcium-Calmodulin-Dependent Protein Kinases/adverse effects/*metabolismCells, CulturedEnzyme Activation/drug effectsFlavonoids/pharmacologyImidazoles/pharmacologyIsoenzymes/adverse effects/*metabolismLipopolysaccharides/*pharmacologyMicroglia/drug effects/*enzymologyMitogens/pharmacologyPyridines/pharmacologyRatsRats, Sprague-Dawley*Salmonella enteritidisTumor Necrosis Factor-alpha/metabolism
PMID
9579682
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Pharmacology
AJOU Authors
주, 일로조, 은혜
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