Artemisinin inhibits lipopolysaccharide-induced interferon-beta production in RAW 264.7 cells: Implications on signal transducer and activator of transcription-1 signaling and nitric oxide production

Abstract

Artemisinin is a well-known anti-malarial drug and has been shown to inhibit nitric oxide (NO) production. In this study, we investigated the effect of artemisinin on lipopolysaccharide (LPS)-induced production of IFN-beta and characterized the potential relationship between artemisinin-mediated inhibition of IFN-beta and NO production. Artemisinin suppressed IFN-beta production and mRNA expression in a dose-dependent manner in LPS-stimulated RAW 264.7 cells. LPS-induced phosphorylation of signal transducer and activator of transcription-1 (STAT-1) was also inhibited by artemisinin treatment in RAW 264.7 cells. In addition, artemisinin suppressed LPS-induced production of NO in RAW 264.7 cells. Further study demonstrated that artemisinin-mediated inhibition of NO production and STAT-1 phosphorylation was reversed by addition of exogenous IFN-beta. Moreover, artemisinin does not affect IFN-beta-induced STAT-1 phosphorylation in RAW 264.7 cells. Collectively, these results suggest that the inhibition of IFN-beta production by artemisinin and concomitant attenuation of STAT-1 activation might be involved in artemisinin-mediated inhibition of NO production in macrophages. (c) 2012 Elsevier B.V. All rights reserved.