Non-Steroidal Anti-Inflammatory Drugs Change Various Inflammatory Mediator-Related Gene Expression In Abeta1-42 Activated Mouse Microglial Cell
Journal of the Korean Geriatrics Society
;
: 130-138, 2007.
Article
in Korean
| WPRIM
| ID: wpr-197987
ABSTRACT
BACKGROUND:
We investigated whether non-steroidal anti-inflammatory drugs(NSAIDs) could influence the expression of a few inflammatory mediator-related genes in amyloid-beta1-42(Abeta42)-activated microglia.METHODS:
BV-2 cells, a murine microglial cell line, were pretreated with a single dose of 20microM of aggregated Abeta42 for 18 hours followed by incubation with ibuprofen(100microM), indomethacin(150microM) or ketorolac(10nM) for 24 hours. Expression of mRNAs for CCL7(beta-chemokine), CXCL2(alpha-chemokine), CCR7(beta-chemokine receptor), interleukin(IL)-1alpha, matrix metalloproteinase(MMP)-3, beta-secretase(BACE1) and cyclooxygenase(COX)-2 gene were measured with quantitative realtime reverse transcriptase(RT)-PCR.RESULTS:
Abeta42 increased expression of mRNAs for CCL7, CXCL2, CCR7, IL-1alpha, MMP-3, BACE1 and COX-2 genes. Administration of each NSAIDs effectively lowered the expression of these genes in Abeta42-activated microglia.CONCLUSION:
NSAIDs inhibit increased expression of a few cytokines, chemokine receptor and inflammatory mediatorrelated protease genes in Abeta42-activated microglia. These data demonstrate a possible mechanism how NSAIDS may decrease the risk and delay the onset of chronic neuroinflammatory process in AD.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
RNA, Messenger
/
Gene Expression
/
Cell Line
/
Anti-Inflammatory Agents, Non-Steroidal
/
Cytokines
/
Microglia
/
Amyloid Precursor Protein Secretases
/
Chemokine CCL7
/
Alzheimer Disease
Limits:
Animals
Language:
Korean
Journal:
Journal of the Korean Geriatrics Society
Year:
2007
Type:
Article
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