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ARTICLE

Simvastatin acts as an inhibitor of interferon gamma-induced cycloxygenase-2 expression in human THP-1 cells, but not in murine RAW264.7 cells

CHANG SEOK LEE¹, YONG JAE SHIN¹, CHEOLHEE WON¹, YUN-SONG LEE², CHUNG-GYU PARK³, SANG-KYU YE^1*, MYUNG-HEE CHUNG¹

1. Department of Pharmacology, Seoul National University College of Medicine, Seoul 110-799, Korea.
2. Department of Pharmacology, Sungkyunkwan University School of Medicine, Suwon 440-746, Korea.
3. Department of Microbiology, Seoul National University College of Medicine, Seoul 110-799, Korea.
* Address correspondence to: Sang-Kyu Ye. E-mail: sangkyu@snu.ac.kr

BIOCELL 2009, 33(2), 107-114. https://doi.org/10.32604/biocell.2009.33.107

Abstract

Cyclooxygenase-2 (COX-2) is a key inflammatory response molecule, and associated with many immune functions of monocytes/macrophages. Particularly, interferon gamma (IFNγ)-induced COX-2 expression appears in inflammatory conditions such as viral infection and autoimmune diseases. Recently, statins have been reported to show variable effects on COX-2 expression, and on their cell and species type dependences. Based on the above description, we compared the effect of simvastatin on IFNγ-induced COX2 expression in human monocytes versus murine macrophages. In a result, we found that simvastatin suppresses IFNγ-induced COX-2 expression in human THP-1 monocytes, but rather, potentiates IFNγ-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 on COX-2 expression, is inactivated by simvastatin in both cells. Our findings showed that simvastatin is likely to suppress IFNγ-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 IFNγ-induced COX-2 expression is differently regulated by simvastatin depending on species specific mechanism.

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