Non-Steroidal Anti-Inflammatory Drugs Change Various Inflammatory Mediator-Related Gene Expression In Abeta1-42 Activated Mouse Microglial Cell.
- Author:
Young Sook CHOI
1
;
Sang Ho KIM
Author Information
1. Department of Pathology, The Catholic University of Korea, College of Medicine, Seoul, Korea. complt@catholic.ac.kr
- Publication Type:Original Article
- Keywords:
Alzheimer's disease;
NSAIDs;
CCL7 chemokine;
CXCL2 protein;
beta-Secretase
- MeSH:
Alzheimer Disease;
Amyloid Precursor Protein Secretases;
Animals;
Anti-Inflammatory Agents, Non-Steroidal;
Cell Line;
Chemokine CCL7;
Cytokines;
Gene Expression*;
Mice*;
Microglia;
RNA, Messenger
- From:Journal of the Korean Geriatrics Society
2007;11(3):130-138
- CountryRepublic of Korea
- Language:Korean
-
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.
