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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Park, Sae-gwang Jung, Won-kyo Choi, Inhak Lee, Chang-min Ko, Jae-hong Park, Cheol Ahn, Soon-cheol Choi, Yung Hyun Seo, Su-kil Lee, Soo-woong Yea, Sung Su Park, Won Sun Choi, Il-whan Lee, Da-young |
| Description | Author Affiliation: Jung WK ( Department of Marine Life Science, Chosun University, Gwangju, Republic of Korea.) |
| Abstract | BACKGROUND AND PURPOSE: Cilostazol is a specific inhibitor of 3'-5'-cyclic adenosine monophosphate (cAMP) phosphodiesterase, which is widely used to treat ischemic symptoms of peripheral vascular disease. Although cilostazol has been shown to exhibit vasodilator properties as well as antiplatelet and anti-inflammatory effects, its cellular mechanism in microglia is unknown. In the present study, we assessed the anti-inflammatory effect of cilostazol on the production of pro-inflammatory mediators in lipopolysaccharide (LPS)-stimulated murine BV2 microglia. EXPERIMENTAL APPROACH: We examined the effects of cilostazol on LPS-induced nuclear factor-kappaB (NF-kappaB) activation and phosphorylation of mitogen-activated protein kinases (MAPKs). KEY RESULTS: Cilostazol suppressed production of nitric oxide (NO), prostaglandin E(2) (PGE(2)) and the proinflammatory cytokines, interleukin-1 (IL-1), tumour necrosis factor-alpha, and monocyte chemoattractant protein-1 (MCP-1), in a concentration-dependent manner. Inhibitory effects of cilostazol were not affected by treatment with an adenylate cyclase inhibitor, SQ 22536, indicating that these actions of cilostazol were cAMP-independent. Cilostazol significantly inhibited the DNA binding and transcriptional activity of NF-kappaB. Moreover, cilostazol blocked signalling upstream of NF-kappaB activation by inhibiting extracellular signal-regulated kinases 1 and 2 (ERK1/2) and c-Jun N-terminal kinase (JNK), but without affecting the activity of p38 MAPK. CONCLUSION AND IMPLICATIONS: Our results demonstrate that suppression of the NF-kappaB, ERK, JNK signalling pathways may inhibit LPS-induced NO and PGE(2) production. Therefore, cilostazol may have therapeutic potential for neurodegenerative diseases by inhibiting pro-inflammatory mediators and cytokine production in activated microglia. |
| ISSN | 00071188 |
| e-ISSN | 14765381 |
| Journal | British Journal of Pharmacology |
| Issue Number | 6 |
| Volume Number | 159 |
| Language | English |
| Publisher | Wiley Online Library(on behalf of The British Pharmacological Society) |
| Publisher Date | 2010-03-01 |
| Publisher Place | Great Britain (UK) |
| Access Restriction | Open |
| Subject Keyword | Anti-Inflammatory Agents, Non-Steroidal Pharmacology Microglia Drug Effects Mitogen-Activated Protein Kinases Antagonists & Inhibitors NF-kappa B Tetrazoles Animals Blotting, Western Cell Line Cell Survival Cyclic AMP Metabolism Dinoprostone Biosynthesis Dose-Response Relationship, Drug Electrophoretic Mobility Shift Assay Inflammation Mediators Immunology Lipopolysaccharides Mice Enzymology Microscopy, Confocal Nitric Oxide Phosphorylation Reverse Transcriptase Polymerase Chain Reaction Signal Transduction Research Support, Non-U.S. Gov't |
| Content Type | Text |
| Resource Type | Article |
| Subject | Pharmacology |
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