Browse
S-Space
College of Medicine/School of Medicine (의과대학/대학원)
Pharmacology (약리학전공)
Journal Papers (저널논문_약리학전공)
Simvastatin acts as an inhibitor of interferon gamma-induced cycloxygenase-2 expression in human THP-1 cells, but not in murine RAW264.7 cells
- Authors
- Lee, Chang Seok; Shin, Yong Jae; Won, Cheolhee; Lee, Yun-Song; Ye, Sang-Kyu; Chung, Myung-Hee; Park, Chung-Gyu
- Issue Date
- 2009-08
- Publisher
- Universidad Nacional de Cuyo
- Citation
- BIOCELL; Vol.33 2; 107-114
- Keywords
- monocyte; SOCS 1/3; macrophage; INF gamma; STAT 1/3
- Abstract
- Cyclooxygenase-2 (COX-2) is a key inflammatory response molecule,,in(] associated with Many immune functions of monocytes/macrophages. Particularly, interferon gamma (IFN gamma)-induced COX-2 expression appears in inflammatory conditions such as viral infection and autoimmune diseases. Recently statins have been reported to show variable effects oil COX-2 expression, and oil their cell and species type dependences. Based on the above description, we compared the effect of simvastatin on IFN gamma-induced COX-2 expression in human monocytes versus murine macrophages. In a result, we found that simvastatin suppresses IFN gamma-induced COX-2 expression in human THP-1 monocytes, but rather, potentiates IFN gamma-induced COX-2 expression in murine RAW264.7 macrophages. However, signal transducer and activator of transcription 1/3 (STAT1/3), known as a transcription factor oil COX-2 expression, is inactivated by simvastatin in both cells. Our findings showed that simvastatin is likely to Suppress IFN gamma-induced COX-2 expression by inhibiting STAT1/3 activation in human THP-1 cells, but not in murine RAW264.7 cells. Thus, we concluded that IFN gamma-induced COX-2 expression is differently regulated by simvastatin depending oil species specific mechanism.
- ISSN
- 0327-9545
- Language
- English
- Files in This Item:
- Appears in Collections:
- College of Medicine/School of Medicine (의과대학/대학원)Pharmacology (약리학전공)Journal Papers (저널논문_약리학전공)
Items in S-Space are protected by copyright, with all rights reserved, unless otherwise indicated.